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Minipress (Prazosin)
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Minipress

Minipress is an effective strong preparation which is taken in treatment of hypertension diseases. Minipress is also helpful in treatment of male prostate enlargement symptoms, congestive heart failure, Raynaud's disease. Minipress acts as anti-hypertension remedy.

Other names for this medication:

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Lisinopril, Amlodipine, Norvasc, Benicar, Metoprolol, Hydrochlorothiazide, Avapro, Losartan

 

Also known as:  Prazosin.

Description

Minipress is created by pharmacy specialists to combat hypertension disease. Target of Minipress is to control level of blood pressure.

Minipress acts as anti-hypertension remedy. Minipress operates by reducing blood pressure.

Minipress is also known as Prazosin, Prazopress, Vasoflex, Hypovase.

Minipress is alpha blocker.

Generic name of Minipress is Prazosin (oral).

Brand name of Minipress is Minipress.

Dosage

You should take it by mouth with water.

It is better to take Minipress 2-3 times a day at the same time with meals or milk.

It is better to start the first Minipress dose when are going to bed.

If you want to achieve most effective results do not stop taking Minipress suddenly.

Overdose

If you overdose Minipress and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Minipress overdosage: feeling lightheaded, rash, weakness, troublesome breathing, pruritus, swelling.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Minipress are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Minipress if you are allergic to Minipress components.

Be careful with Minipress if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Minipress if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Minipress if you have allergies to medicines, foods, or other substances.

Be careful with Minipress if you have liver or kidney disease, heart failure, low blood pressure, narcolepsy, prostate cancer.

Be careful with Minipress if you take muscle relaxants as carisoprodol; anti-anxiety drugs as diazepam; anti-seizure drugs as carbamazepine; tranquilizers; sleep medicines as sedatives; antihistamines as diphenhydramine; verapamil; psychiatric medicines as tricyclic antidepressants (amitriptyline), phenothiazines (chlorpromazine); sexual function problems drugs as vardenafil, sildenafil, tadalafil; narcotic pain relievers as codeine; beta blockers as metoprolol, propranolol, atenolol.

Avoid machine driving.

Use Minipress with great care in case you want to undergo an operation (dental or any other).

Avoid alcohol.

Minipress can be not safety for elderly people.

Try to be careful with sunbeams. Minipress makes skin sensitive to sunlight. Protect skin from the sun.

Do not stop taking Minipress suddenly.

minipress drug information

This article attempts to put into clinical context the recently described effects of certain alpha(1)-AR on prostate cell dynamics (i.e., proliferation and apoptosis). RESULTS AND CONCLUSIONS There is good evidence that certain alpha(1)-AR antagonists, in addition to affecting stromal smooth muscle, have effects on prostatic apoptosis that contribute to the overall clinical profile. Furthermore, this is not a class effect and may be restricted to balanced quinazoline alpha blockers (BQABs), such as terazosin.

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The majority of smokers relapse during the acute withdrawal phase when withdrawal symptoms are most severe. The goal of the present studies was to investigate the role of corticotropin-releasing factor (CRF) and noradrenergic transmission in the central nucleus of the amygdala (CeA) in the dysphoria associated with smoking cessation. It was investigated if blockade of CRF1 receptors, blockade of α1-adrenergic receptors, or stimulation of α2-adrenergic receptors in the CeA diminishes the deficit in brain reward function associated with nicotine withdrawal in rats. Nicotine dependence was induced by implanting minipumps that delivered a nicotine solution. Withdrawal was precipitated with the nicotinic acetylcholine receptor antagonist mecamylamine. A discrete-trial intracranial self-stimulation procedure was used to assess the negative affective aspects of nicotine withdrawal. Elevations in brain reward thresholds are indicative of a deficit in brain reward function. In all the experiments, mecamylamine elevated the brain reward thresholds of the rats chronically treated with nicotine and did not affect the brain reward thresholds of the saline-treated control rats. Intra-CeA administration of the CRF1 receptor antagonist R278995/CRA0450 completely prevented the mecamylamine-induced elevations in brain reward thresholds in the nicotine-treated rats and did not affect the brain reward thresholds of the saline-treated control rats. R278995/CRA0450 has also been shown to block sigma-1 receptors but there is no evidence that this could affect negative mood states. Intra-CeA administration of the α1-adrenergic receptor antagonist prazosin or the α2-adrenergic receptor agonist clonidine did not affect the brain reward thresholds of the nicotine or saline-treated rats. These studies suggest that CRF1 receptor antagonists may diminish the dysphoria associated with smoking cessation by blocking CRF1 receptors in the CeA.

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The prostate gland is a rich source of alpha1-adrenergic receptors (alpha1-ARs). alpha1-AR antagonists are commonly used in the treatment of benign prostatic hyperplasia symptoms, due to their action on smooth muscle cells. However, virtually nothing is known about the role of alpha1-ARs in epithelial cells. Here, by using two human prostate cancer epithelial (hPCE) cell models - primary cells from resection specimens (primary hPCE cells) and an LNCaP (lymph node carcinoma of the prostate) cell line - we identify an alpha1A subtype of adrenergic receptor (alpha1A-AR) and show its functional coupling to plasmalemmal cationic channels via direct diacylglycerol (DAG) gating. In both cell types, agonist-mediated stimulation of alpha1A-ARs and DAG analogues activated similar cationic membrane currents and Ca(2+) influx. These currents were sensitive to the alpha1A-AR antagonists, prazosin and WB4101, and to transient receptor potential (TRP) channel blockers, 2-aminophenyl borate and SK&F 96365. Chronic activation of alpha1A-ARs enhanced LNCaP cell proliferation, which could be antagonized by alpha1A-AR and TRP inhibitors. Collectively, our results suggest that alpha1-ARs play a role in promoting hPCE cell proliferation via TRP channels.

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The total IPSS, IPSS-QoL, and OABSS decreased significantly in both tenoxicam plus doxazosin group and doxazosin alone group compared with baseline (P < .01). Also, Q(max) and AFR significantly improved in both groups (P < .01). The improvements in IPSS, IPSS-QoL, and OABSS were significantly better in patients treated with combination therapy (P < .05).

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1. The effects of cooling on the response of the rabbit central ear (cutaneous) and femoral (non-cutaneous) arteries to stimulation of adrenoceptors and the role of the endothelium in these effects, were studied in 2 mm long cylindrical segments. 2. Concentration-response curves for noradrenaline (10(-9)-3 x 10(-4) M), phenylephrine (alpha 1-adrenoceptor agonist, 10(-9)-3 x 10(-4) M) and B-HT 920 (alpha 2-adrenoceptor agonist, 10(-7)-10(-3) M) were recorded isometrically in arteries with and without endothelium at 37 degrees C and at 24 degrees C (cooling). To analyze further the endothelial mechanisms in the responses to adrenoceptor stimulation during cooling, the effects of the adrenoceptor agonists on ear arteries in the presence of NG-nitro-L-arginine methyl esther (L-NAME) (10(-5) M) were also determined. 3. In every condition tested, the three adrenoceptor agonists produced a concentration-dependent arterial contraction and the order of potency in ear and femoral arteries was noradrenaline greater than or equal to phenylephrine greater than B-HT 920. The response of ear and femoral arteries to phenylephrine or B-HT 920 was blocked by prazosin (10(-6) M). Yohimbine (10(-6) M) decreased slightly the response of ear arteries and increased that of femoral arteries to B-HT 920. 4. The sensitivity of both ear and femoral arteries to the three adrenoceptor agonists was significantly lower at 24 degrees C than at 37 degrees C. 5. In ear arteries, endothelium removal or treatment with L-NAME did not influence the response at 37 degrees C, but did increase it during cooling to adrenoceptor stimulation.In femoral arteries, endothelium removal increased the sensitivity to noradrenaline and, especially, to B-HT 920 at 37 degrees C, but did not affect the response at 24 degrees C.6. The results suggest that: (a) rabbit ear and femoral arteries are equipped mainly with alpha 1-adrenoceptors;(b) at 37 degrees C, the contraction of the ear artery to adrenoceptor agonists is mostly endothelium-independent, and in the femoral artery the contraction to alpha 2-adrenoceptor activation is endothelium-dependent; (c) cooling inhibits the contraction to adrenoceptor agonists in both ear and femoral arteries: in the ear artery probably by increasing the availability of endothelial nitric oxide, but in the femoral artery by depressing the sensitivity of alpha-adrenoceptors in the smooth musculature.7. The results suggest that the endothelium may modulate the adrenoceptor response of cutaneous arteries during changes in temperature.

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We would like to suggest that LIHTN may better be managed by alpha blockers compared with converting enzyme inhibitors.

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Arterial Hypertension (AHT) has been studied in 77 patients (p) subjected to hemodialysis (HD). Mean age (mag) was 61 years (y), range 84y-25y; 66% were males. The underlying etiology was glomerular in 19%, tubulo-interstitial in 18%, congenital in 18%, vascular in 19% and diabetic in 26%.

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To observe the effects of (-)doxazosin(DOX), (+)DOX and (+/-)DOX on serum lipid levels and the mortality rates of the rabbits fed by an atherogenic diet.

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Alpha-1 and alpha-2 adrenergic receptors were localized in developing cat visual cortex by using [3H]prazosin and [3H]rauwolscine, respectively as selective ligands. The effects of neuronal input on the development of the two receptor subtypes were also studied in animals with lesions at various sites within the central visual pathways. Binding densities for both ligands increased during the first few postnatal weeks and declined thereafter. For both receptor subtypes, the highest concentration of binding sites was found in the subplate zone of the cortex in neonatal animals. Both ligands showed their highest concentrations in cortical layer IV beginning at postnatal day 30 and in the superficial cortical layers in adulthood. However, the developmental redistribution of alpha-1 receptors began at earlier ages than that of the alpha-2 sites. The alpha-1 sites were still concentrated in the subplate zone up to 60 days postnatal, while the alpha-2 sites in this region disappeared much earlier. Receptor binding densities were also examined in animals with quinolinic acid lesions within cortex, lesions of the lateral geniculate nucleus and lesions of the optic tract. The results indicate that both alpha-adrenoceptor subtypes were mainly located on cortical cells, and that the absence of neuronal activity during development resulted in a reduction of the binding density for both subtypes in the visual cortex. An additional major reduction in alpha-2 but not alpha-1 binding sites was observed following the lateral geniculate nucleus lesion, suggesting that the development of alpha-2 receptors is also dependent on input from the lateral geniculate nucleus. Removal of the lateral geniculate nucleus early in life resulted in a significant increase in alpha-1 receptors in the subplate region, indicating that receptor densities in this zone may be negatively regulated by the lateral geniculate nucleus afferents. These results show that adrenergic receptors reorganize during postnatal cortical development with a strong temporary concentration in the subplate zone. The reorganization process is heavily influenced by cortical inputs.

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Brimonidine is a relatively selective alpha-2 adrenoceptor agonist that is being developed for the treatment of glaucoma. Because brimonidine is chemically related to clonidine and has affinity for the nonadrenergic imidazoline receptor, its ocular effects may be unrelated to alpha-2 receptor activation. The objective of this study was to determine the pharmacology of the intraocular pressure (IOP) response to brimonidine in rabbits and monkeys and the side effects (miosis, cardiovascular depression) in monkeys. Conscious albino rabbits and cynomolgus monkeys were pretreated topically with the following receptor antagonists: rauwolscine (alpha-2), idazoxan (alpha-2, imidazoline), SKF 105854 (vascular postjunctional alpha-2), and prazosin (alpha-1). Intraocular pressure, pupil size, or blood pressure/heart rate was monitored noninvasively for 6 hours following dosing. Binding experiments were performed using [3H]brimonidine in membrane preparations from rabbit iris/ciliary body and from monkey cerebral cortex and brain stem. In rabbits, the ocular hypotensive response to brimonidine was unilateral and was inhibited by rauwolscine > idazoxan > SKF 105854 = prazosin; this ranked order of potency correlated with displacement of [3H]brimonidine in the rabbit iris/ciliary body. In monkeys, brimonidine decreased IOP bilaterally and suppressed cardiovascular function suggesting a CNS site of action. Intraocular pressure and cardiovascular responses to brimonidine were inhibited by idazoxan > rauwolscine > SKF 105854 = prazosin; a similar profile was obtained for displacement of [3H]brimonidine in monkey brain tissue. Both rauwolscine and idazoxan inhibited the miotic response to brimonidine in monkeys. Taken together, these results indicate that brimonidine stimulates an ocular alpha-2 adrenoceptor to decrease IOP in the rabbit and a CNS imidazoline receptor to decrease IOP, blood pressure, and heart rate in the cynomolgus monkey. The miotic response in the monkey is mediated by an alpha-2 adrenoceptor. The alpha-1 and vascular postjunctional alpha-2 adrenoceptors do not appear to play a role in mediating these responses.

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Norepinephrine, through alpha(1)-adrenoceptors, reduces current amplitude in a concentration-dependent way, with no effects on current kinetics or voltage dependence of inactivation. Diabetes reduces current amplitude and accelerates its inactivation process. Norepinephrine also reduces current amplitude in diabetic cells; however diabetes shifts to the right the concentration-response curve and reduces the maximum effect of the neurotransmitter.

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This study showed that terazosin inhibited not only prostate cancer cell growth but also colony-forming ability, which is the main target of clinical treatment. On the other hand, alfuzosin and phenoxybenzamine have no effect on cell viability and colony forming ability of PC-3 and DU145. In addition, the terazosin inhibits cell growth through G(1) phase cell cycle arrest.

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The inhibition of the norepinephrine-induced aortic contraction by melatonin was more potent in spontaneously hypertensive than it was in Wistar-Kyoto rats. The inhibition of the norepinephrine-induced formation of inositol phosphate by 0.3-300 micromol/l melatonin was also greater in smooth muscle cells from spontaneously hypertensive rats than it was in those cells from Wistar-Kyoto rats. In contrast, the inhibition of the norepinephrine-induced formation of inositol phosphate in smooth muscle cells from spontaneously hypertensive and Wistar-Kyoto rats by 2-iodomelatonin, an agonist of melatonin receptors, was not different. Prazosin, but not yohimbine, eliminated or partially inhibited the norepinephrine-induced formation of inositol phosphate in smooth muscle cells from Wistar-Kyoto rats or from spontaneously hypertensive rats, respectively. In the presence both of prazosin and of melatonin, the norepinephrine-induced production of inositol phosphate was abolished in smooth muscle cells from spontaneously hypertensive rats. Furthermore, superoxide dismutase significantly inhibited the norepinephrine-induced aortic contraction and formation of inositol phosphate in smooth muscle cells from spontaneously hypertensive rats, but not in those cells from Wistar-Kyoto rats. In contrast, catalase had no effect on the norepinephrine-induced formation of inositol phosphate and vascular contraction either in cells from spontaneously hypertensive rats or in cells from Wistar-Kyoto rats. Hypoxanthine-xanthine oxidase induced formation of more inositol phosphate in smooth muscle cells from spontaneously hypertensive rats than it did in those from Wistar-Kyoto rats. Melatonin and superoxide dismutase similarly inhibited the hypoxanthine-xanthine oxidase-induced formation of inositol phosphate more in cells from spontaneously hypertensive rats than it did in those from Wistar-Kyoto rats. However, melatonin had no effect either on basal or on the forskolin-induced formation of cyclic AMP in smooth muscle cells from rats of both strains.

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Administrative VA data from fiscal years 1999 through 2009 were used to identify veterans with PTSD using ICD-9 codes extracted from inpatient discharges and outpatient encounters. Prescribing of antidepressants, antipsychotics, and hypnotics was determined for each fiscal year using prescription drug files.

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This evidence challenges conventional knowledge of the mechanism of action of alpha(1)-adrenoceptor antagonists, and points to a new therapeutic value for these drugs by providing a differential molecular basis for their anti-tumor efficacy. The present review focuses on the characterization of the apoptotic/anti-angiogenic effect of quinazoline-based alpha(1)-adrenoceptor antagonists against prostate cancer cells and discusses the clinical significance of this action in the prevention and treatment of prostate cancer.

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These results demonstrate that the apoptotic effect of Doxazosin on human prostatic stromal cells is mediated through an autocrine production of TGF-beta1.

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We have shown previously that noradrenaline (NA) stimulated or inhibited the release of corticotropin-releasing hormone (CRH) according to the availability of adrenal steroids. The aim of the present work was to examine whether the changes in the NA modulation of CRH release from hypothalamic neurons result from a steroid-induced plasticity of the adrenergic transduction pathways. From anterior hypothalamic slices cultured in standard medium (i.e., containing adrenal steroids at a final dilution of 61 +/- 9 ng/ml), (a) the stimulatory effect of NA on CRH release was reversed in a dose-dependent manner by increasing concentrations of the alpha1-adrenoreceptor antagonist prazosin, (b) activation of protein kinase C by acute treatment with phorbol 12-myristate 13-acetate (0.5 microM, 1 h) mimicked NA stimulation of CRH secretion, and (c) the activation of L-type Ca2+ channels by Bay K 8644 also produce an increased CRH secretion. In contrast, the inhibitory effect of NA on CRH secretion from slices cultured in steroid-free medium was markedly reversed by the alpha2-adrenoreceptor antagonist yohimbine, by pretreatment with pertussin toxin, or by the addition of 4-aminopyridine, a K+-channel blocker. Acute treatment with phorbol 12-myristate 13-acetate did not change the inhibitory NA effect. Moreover, all these effects were reversed by daily corticosterone supplementation, for as long as they were tested. These results are consistent with a steroid-dependent change in the nature of adrenergic receptors and its associated transduction pathways involved in the regulation of CRH secretion in the hypothalamus.

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1. The vasoconstrictor effects of noradrenaline applied to the intimal and adventitial surfaces of perfused segments of rat tail artery in the presence and absence of endothelium were studied. 2. Noradrenaline was about six times more potent as a vasoconstrictor when applied to the intimal than to the adventitial surface. Cocaine (25 mumol/L) enhanced responses to adventitial noradrenaline to a greater extent than those to intimal noradrenaline. A high concentration of propranolol (1 mumol/L) had a similar effect. 3. The vasoconstriction elicited by adventitial noradrenaline declined from a peak whereas that to intimal noradrenaline remained steady. A low concentration of propranolol (0.1 mumol/L) abolished the decline in the response to adventitial noradrenaline. 4. The alpha 1- and alpha 2-adrenoceptor antagonists prazosin (1 nmol/L) and idazoxan (100 nmol/L) significantly reduced responses to intimal and adventitial noradrenaline in the presence or absence of endothelium. 5. Removal of endothelium enhanced responses to intimal but not adventitial noradrenaline. Idazoxan produced a significantly greater reduction of responses to noradrenaline in the absence than in the presence of endothelium, and was more effective against intimal than adventitial noradrenaline. Similar effects were produced by the nitric oxide synthase inhibitor L-NAME (30 mumol/L). 6. It was concluded that noradrenaline acts on both alpha 1- and alpha 2-adrenoceptors to produce vasoconstriction: the alpha 1-adrenoceptors appear to be uniformly distributed, whereas alpha 2-adrenoceptors are located nearer the intima. Intimal noradrenaline also acts on endothelial alpha 2-adrenoceptors to release EDRF which counteracts the vasoconstrictor action of noradrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)

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The response to four different vasodilators, and cotreatment with blockers of NO and prostaglandin synthesis, was compared. Femoral artery blood flow was correlated with capillary-to-fibre ratio (C:F) and protein levels of putative angiogenic compounds.

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Canine narcolepsy is an animal model of the human rapid eye movement sleep disorder. Dogs exhibit bouts of sleep attacks and muscle atonia (cataplexy) that are induced by emotions and thought to be abnormal rapid eye movement sleep episodes. We have previously demonstrated that cataplexy is strongly inhibited by increases in noradrenergic activity. This effect is mediated through central alpha 1-adrenoceptors, presumably of the alpha 1B subtype. In this study, we demonstrate with the canine model that SDZ NVI-085, a new compound with alerting effects, is a potent anticataplectic agent that may act through stimulation of an alpha 1-adrenoceptor subtype.

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We found no association between modified-release doxasozin use and fractured hip/femur, humerus or wrist in those without a recent history of falls, or trauma.

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Experiments were performed on normotensive rats exposed to vitamin D deficient and control diets from the 22nd to the 180th day of age. In 60-120- and 180-day-old rats. The following parameters were evaluated: a) The vasomotor responses elicited by receptor agonists in the absence and in the presence of the respective antagonists [L-norepinephrine (NE) before and 5 min after prazosin; L-isoprenaline (I) before and 5 min after DL-propranolol; L-dopamine (DA) before and 5 min after L-sulpiride or SCH 23390 or chlorpromazine; acetylcholine (Ach) before and 5 min after atropine; histamine (H) before and after chlorpheniramine; 5-hydroxytryptamine (5-HT) before and 5 min after methysergide or ketanserin]; by carotid-sinus baroreceptor stimulation (CO) before and 5 min after hexamethonium, and by electrical stimulation of the vagus peripheral head (V) before and after atropine; b) Reflex tachycardia elicited by bilateral carotid occlusion (CO) (for 40 sec) and by sodium nitroprusside; c) Catecholamine (norepinephrine, epinephrine) and arginine-vasopressin plasma levels; d) Cholesterol, triglyceride and electrolyte (Na+, K+, Cl-, Ca2+) serum levels. Our results showed that vitamin D deficient diets induced a decrease in pressor responses to NE and CO, and an increase in hypotensive responses to I, DA, Ach, H, 5-HT and V. Changes of arterial blood pressure, heart rate, catecholamine and arginine-vasopressin plasma levels were not observed. Cholesterol, triglyceride and electrolyte (Na+, K+, Cl-) serum levels were not modified, while Ca2+ serum levels decreased. In conclusion, our data suggest that vitamin D depletion can induce changes of pressor and depressor vasomotor responses and suppose a direct role for vitamin D in regulating vasomotor reactivity.

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The effects of microiontophoresis of norepinephrine and epinephrine were examined on the spontaneous neuronal activity of single neurons in the nucleus tractus solitarius (NTS) in urethan-anesthetized rats. Neuronal responses to catecholamine iontophoresis were examined in the absence and presence of the alpha 1-adrenergic antagonist, prazosin, and the alpha 2-antagonist, idazoxan, to characterize the subtypes of alpha-adrenergic receptors mediating catecholamine action in this important autonomic nucleus. Norepinephrine produced inhibitions in firing, which were blocked primarily by idazoxan, whereas epinephrine-induced neuronal inhibitions were blocked by either prazosin or idazoxan. Inhibitions of spontaneous firing were also produced by iontophoresis of methoxamine, an alpha 1-selective agonist, or the alpha 2-selective agonist clonidine in all neurons that were tested. Neuronal responses to methoxamine were blocked selectively by prazosin, whereas the effects of clonidine were antagonized selectively by idazoxan. These data provide evidence at the level of the single unit that catecholamines may affect activity in the NTS via interactions with both alpha 1- and alpha 2-adrenergic receptors.

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Doxazosin (-4 mg) effectively decreased BP in awake and 24-hour periods without a significant improvement during sleep. A double dose of the drug added little benefit. Optimal BP was reached by an insufficient number of patients. Doxazosin proved to have a good tolerance and safe profile. This results suggest that doxazosin should be considered a good add-on treatment to other antihypertensive drugs in RT.

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The concept of alpha1-adrenoceptor subtypes was first suggested in the mid 1980s on the basis of the different affinities of certain alpha1-adrenoceptor preparations for the alpha-adrenoceptor agonist, oxymetazoline, and the antagonists, WB4101 and phentolamine. Subsequent characterization of alpha1-adrenoceptors using radioligand binding and functional studies has led to the identification of three native prazosin high-affinity alpha1-adrenoceptor subtypes designated alpha1A, alpha1B and alpha1D, corresponding to the three alpha1-adrenoceptor subtypes (alpha1a, alpha1b and alpha1d) isolated by molecular cloning techniques. Since each of these three subtypes exhibits similar affinity for the selective alpha1-adrenoceptor antagonist, prazosin, [3H]prazosin can be used as a convenient probe to evaluate the interaction of compounds with these adrenoceptor subtypes. Considerable clinical experience over the last few years has provided convincing evidence to support the effectiveness of alpha1-adrenoceptor blockade in the treatment of bladder obstruction due to benign prostatic hyperplasia (BPH). The distribution of alpha1-adrenoceptors in the human prostate tissue has shown that the predominant cloned alpha1-adrenoceptor subtype characterized by RNAase protection assays corresponds to the alpha1a-subtype, formerly classified as alpha1c. Many of the alpha1-antagonists currently prescribed in the treatment of BPH do not exhibit in vitro selectivity between alpha1a-, alpha1b- and alpha1d-subtypes and yet they have good clinical tolerance in terms of low incidence of cardiovascular effects. One possibility to account for these findings is that another alpha1-adrenoceptor subtype could be implicated in human prostatic smooth muscle contraction. A recent report, although confirming the presence of an alpha1a-subtype in human prostate, suggested that an alpha1-adrenoceptor subtype with lower affinity for prazosin, designated alpha1L, which has not been cloned yet, is in fact the predominant alpha1-subtype involved in the contractile response of human prostatic smooth muscle to noradrenaline.

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minipress 6 mg 2016-03-07

We previously reported that caffeic acid produce antidepressive- and/or anxiolytic-like effects in two different types of stress models. It has recently been reported that caffeic acid affects the alpha1A-adrenoceptor system. The present study examined whether the alpha1A-adrenoceptor system is buy minipress involved in the antidepressive- and/or anxiolytic-like effects of caffeic acid. Caffeic acid reduced the duration of immobility and freezing of mice produced by forced swimming and conditioned fear stress, respectively. These effects of caffeic acid were suppressed by the alpha1- and alpha1A-adrenoceptor antagonists. However, caffeic acid did not alter the binding of [3H]prazosin to alpha1A-adrenoceptor in mouse cortical membranes. These results suggest that indirect modulation of the alpha1A-adrenoceptor system may be involved in the antidepressive- and/or anxiolytic-like effects of caffeic acid.

minipress overdose symptoms 2016-06-30

It has long been recognised that neural factors are of considerable importance in lower urinary tract function. Whilst buy minipress reduction in the bulk of the human prostate is feasible, experience on this therapeutic approach proved to be disappointing. Existing trial data with the agent finasteride are reviewed. A number of formulations derived from plant extracts have been advocated but their mechanism of action remain largely obscure and there is a dearth of placebo controlled information to support their efficacy. Experience over the last 10 years has demonstrated efficacy with the use of alpha adrenoceptor blockade in the management of BPH. Alpha adrenoceptor antagonists relax the prostatic smooth muscle by interrupting the sympathetic pathway at the receptor level. Recent developments in this field include the recognition that there are alpha I adrenoceptor subtypes. The functional adrenoceptor in the human prostate is predominantly the alpha IA - subtype. Of the alpha 1-adrenoceptor antagonists only tamsulosin discriminates between the alpha 1-adrenoceptor subtypes. Alpha 1-blockers should be used in first-line medical therapy for BPH and 5-alpha-reductase inhibitors reserved for those patients in whom alpha-blocker therapy fails. Alpha I-blockers such as doxazosin, tamsulosin, terazosin, alfuzosin are effective in the treatment of BPH both in younger and in older men. The drugs are well tolerated. The majority of side effects were classified as minor and mild. The most common complaints, as with other alpha-blockers, are dizziness, fatigue and headache, and these are often transient. In contrast, finasteride can lead to impotence, reduced libido. gynaecomastia or ejaculatory disorders. Men with small prostates may not be suitable candidates for finasteride therapy.

minipress 2 mg 2015-09-19

The contractile response of human prostate adenomas to KCl, phenylephrine (alpha 1 adrenergic agonist), UK 14304 (alpha 2 adrenergic agonist), and carbachol (muscarinic cholinergic agonist) was evaluated in tissue specimens obtained from men with symptomatic and asymptomatic BPH. Prostate specimens were obtained from 5 men with asymptomatic BPH undergoing cystoprostatectomy, 11 men with symptomatic BPH undergoing open prostatectomy, and 11 men with symptomatic BPH undergoing transurethral resection of the prostate (TURP). Quantitative symptom score analysis and urinary flow rate determination documented the absence of bladder outlet obstruction in men undergoing cystoprostatectomy and confirmed the presence of bladder outlet obstruction in men undergoing prostatectomy. The magnitude of the contractile response (Emax) and the potency of phenylephrine-induced contractions (EC50) in prostatic preparations obtained from men with symptomatic and asymptomatic BPH were similar. The IC50 for the inhibition of buy minipress phenylephrine-induced contractions by prazosin was 3.2 nM, confirming that phenylephrine-induced contraction in the human prostate is mediated by the alpha 1 adrenoceptor. The contractile responses of prostate adenomas to muscarinic cholinergic and alpha 2 agonists were negligible. This study demonstrates that the development of bladder outlet obstruction in men with BPH is not related to alterations in the functional response of the smooth muscle component of the prostate adenoma.

minipress dosage 2017-10-08

We implanted rats with a VNS electrode and stimulator. We used the selective noradrenergic toxin DSP-4 to lesion NE neurons of the locus coeruleus. We recorded dorsal raphe 5-HT buy minipress neurons under chloral hydrate anesthesia. We recorded hippocampus CA(3) pyramidal neurons using 5-barreled iontophoretic pipettes.

tab minipress dosage 2016-01-27

To evaluate the clinical role of an alpha(1a-1d)-specific blocker in the medical expulsive buy minipress therapy of symptomatic lower ureteral stones.

minipress tablets dose 2017-05-14

This multicentre, single-blind, randomized trial compared terazosin and tamsulosin over 4 weeks, in 61 patients with symptomatic BPH randomly assigned to terazosin (n = 31) or tamsulosin (n = 30). Terazosin 0.5 mg twice daily was administered for 2 weeks, followed by 1 mg twice daily for 2 weeks. Tamsulosin (0.2 mg) was administered once buy minipress daily for 4 weeks. Symptoms were evaluated using the International Prostate Symptom Score (IPSS), and quality of life (QOL) was assessed subjectively before treatment, and again after 2 and 4 weeks of treatment. Objective measurements taken before and after the treatment period were the maximum (Qmax) and average (Qave) urinary flow rates, and the percentage residual urine volume. Improvement was defined as a 25% decrease from baseline in IPSS, > 1 point increase in QOL score, and > 2.5 mL/s increase in Qmax. Adverse reactions potentially related to the study drugs were recorded throughout the treatment period.

minipress tab 2016-10-11

1. The pharmacology of various agonists and antagonists was studied in the human isolated cystic artery. 2. The estimated pA2s for the alpha 1-adrenoceptor antagonist prazosin against the alpha-adrenoceptor agonists phenylephrine, alpha-methylnoradrenaline and noradrenaline were not significantly different. Similar results were seen for estimated pA2s of the alpha 2-adrenoceptor antagonist yohimbine against these same agonists. Equivalent responses to exogenous noradrenaline and to transmural electrical stimulation were blocked to the same degree by an antagonist with alpha 1-adrenoceptor blocking properties (prazosin). Responses to transmural electrical stimulation, however, tended to be more resistant than equivalent responses to exogenous noradrenaline to blockade by antagonists with alpha 2-adrenoceptor blocking properties (phentolamine, yohimbine). 3. Relaxation to isoprenaline was observed in partially contracted arterial strips using isoprenaline concentrations of up to 10(-6) M, but cumulative addition of higher concentrations of isoprenaline sometimes then evoked a contraction from the relaxation nadir. The relaxation effect of isoprenaline was antagonized by propranolol (10(-5) M). 4. These findings suggest buy minipress the human cystic artery has almost exclusively alpha 1-adrenoceptors postjunctionally, although prejunctional alpha 2-adrenoceptors may be present; and, it also has some postjunctional beta-adrenoceptors which mediate relaxation.

minipress drug class 2017-04-08

Our results show that: ( buy minipress 1) short-term dehydration can be used as a model to study cardiovascular responses associated with water intake in rats; and (2) the sympathetic nervous system and vascular smooth muscle alpha1-adrenoceptors are involved in the pressor response to water intake by dehydrated rats.

minipress overdose 2016-12-31

Seventeen adult cats were chronically implanted with electrodes for polygraphic recordings in order to assess the role of catecholamines in the arousal effects of oral administrations of modafinil, a presumed noradrenergic agonist, and amphetamine, a well-known catecholamine-releasing agent. Whereas both modafinil (1, 2.5 and 5 mg/kg) and amphetamine (0.25, 0.5 and 1 mg/kg) caused a significant and dose-dependent increase in wakefulness and brain temperature, amphetamine, but not modafinil, elicited marked signs of behavioral excitation. Pretreatments with alpha-methyl-DL-p-tyrosine methyl ester (50 mg/kg, i.p.), an inhibitor of catecholamine synthesis, almost completely prevented the effects of amphetamine (0.25 and 1 mg/kg), but only slightly reduced the duration of the waking effect of modafinil (2.5 and 5 mg/kg). Pretreatments with phentolamine (10 mg/kg, i.p.), prazosin (1.5 mg/kg, per os) and propranolol (5 mg/kg, i.p.), an alpha-, alpha 1- and beta-receptor antagonist, respectively, attenuated significantly the arousal effect of modafinil (1 mg/kg buy minipress , the same as below) but not of amphetamine (0.25 mg/kg, the same as below). Intraperitoneal injections of haloperidol (0.5 mg/kg), a dopamine-receptor antagonist, blocked significantly the arousal of amphetamine but not of modafinil. The effects of both modafinil and amphetamine were enhanced by a pretreatment with yohimbine (1 mg/kg, i.p.), an alpha 2-receptor antagonist. These results suggest that the arousal effect of modafinil does not depend on the availability of the endogenous catecholamines but results from an enhancement of alpha 1- and beta-receptor activity and that the waking and behavioral effects of amphetamine may be mainly due to an increase in dopamine release.

minipress generic name 2015-02-18

Doxazosin (mean dose 11 mg) given once daily in combination with 100 mg atenolol (n = 44) was compared with placebo and atenolol (n = 43) in a double-blind, multicenter study in patients with mild to moderate essential hypertension. In the atenolol/doxazosin-treated group, standing blood pressure significantly decreased by 17.0/12.3 mm Hg compared to 6.2/6.7 mm Hg in the atenolol/placebo group whereas supine blood pressure decreased by 13.2/9.8 mm Hg and 9.2/6.0 mm Hg, respectively in the two groups. Serum lipids did not change significantly in either group. The majority of side-effects reported were mild and transient. This study confirms that doxazosin may be safely buy minipress combined with a beta-blocker. Doxazosin proved to be well tolerated and effective in patients with blood pressure refractory to atenolol alone.

minipress medication 2016-10-20

Systolic arterial pressures of conscious rats were determined by using the indirect buy minipress tail-cuff method.

minipress capsules 2015-07-15

Cost-effectiveness was buy minipress measured as the cost in Spanish Ptas per life year gained (LYG) in 1998 in individuals aged 40 to 69 years with moderate/severe hypertension (>= 105 mmHg) and mild hypertension (95-104 mmHg). We evaluated hydrochlorothiazide (diuretic), propranolol (-blocker), nifedipine (calcium antagonist), captopril (angiotensin-converting-enzyme inhibitor) and prazosin (*-adrenergic blocker).

minipress xl dose 2017-12-13

The effect of TCM is weaker than that of buy minipress WM in the assessment of the IPSS score (p<0.05), and both treatments are similar in the prostate volumes, the maximum UFR and the QOL assessments (p>0.05), as well as in the effective number of urethra-related or non-urethra-related symptoms before and after treatment (p>0.05). By comparing the linear regression models, different urethra-related and non-urethra-related symptom patterns associated with TCM and WM therapies are detected for four assessments, especially for the prostate volume assessment (p<0.01).

minipress medicine 2016-01-14

Abnormalities in activity of the endothelin (ET) system have been widely reported in a number of cardiovascular disease states such as hypertension and heart failure. Although the vascular responses to ET are well established, the interaction between ET and other important modulators of blood pressure, such as the sympathetic nervous system, are less understood. Previous reports implicate ET signaling through ET type B (ETB) receptors in increasing neuronal activity. Therefore, we hypothesized that activation of ETB receptors on sympathetic nerves would increase blood pressure through an adrenergic-mediated mechanism. Thus, we used anesthetized ETB-deficient rats, which only express functional ETB receptors on adrenergic neurons, and genetic controls, which express functional ETB receptors in vascular tissue and kidney epithelium. We determined the pressor response to the selective ETB receptor agonist sarafotoxin c ( Trileptal 2400 Mg S6c). Separate groups of rats were treated with the α1-adrenergic receptor antagonist prazosin or the β-adrenergic receptor antagonist propranolol to elucidate the role of adrenergic signaling in mediating the blood pressure response. We observed a dose-dependent pressor response to S6c in ETB-deficient rats that was reversed by prazosin treatment and augmented by propranolol. In genetic control rats, the effects of S6c on sympathetic neurons were mostly masked by the direct activity of ETB receptor activation on the vasculature. Heart rate was mostly unaffected by S6c across all groups and treatments. These results suggest that ETB activation on sympathetic neurons causes an increase in blood pressure mediated through α1-adrenergic receptor signaling.

minipress ptsd dosage 2015-09-09

The objective of this open randomized clinical study was to compare the short-term efficacy and safety of three alpha-1 blockers, prazosin, terazosin and tamsulosin, in the treatment of lower Benicar Generic Cost urinary tract symptoms (LUTS) associated with benign prostatic hyperplasia (BPH).

minipress dosage forms 2017-09-03

HhAntag691 (GDC-0449), a low-molecular weight inhibitor of the tumor-promoting hedgehog (Hh) signaling pathway, has been used to treat medulloblastoma in animal models and has recently entered clinical trials for a variety of solid tumors. Here, we show that HhAntag691 inhibits multiple ATP-binding cassette (ABC) transporters. ATP-binding cassette transporters are within a family of membrane proteins, the overexpression of which is associated with multidrug resistance, a major impediment to successful cancer treatment. HhAntag691 is a potent inhibitor of two ABC Prevacid Ready Tab transporters, ABCG2/BCRP and ABCB1/Pgp, and is a mild inhibitor of ABCC1/MRP1. In ABCG2-overexpressing HEK293 cells, HhAntag691 increased retention of the fluorescent ABCG2 substrate BODIPY-prazosin and resensitized these cells to mitoxantrone, an antineoplastic ABCG2 substrate. In Madin-Darby canine kidney II cells engineered to overexpress Pgp or MRP1, HhAntag691 increased the retention of calcein-AM and resensitized them to colchicine. HhAntag691 also resensitized human non-small cell lung carcinoma cells NCI-H460/par and NCI-H460/MX20, which overexpress ABCG2 in response to mitoxantrone, to mitoxantrone, and to topotecan or SN-38. The IC(50) values of HhAntag691 for inhibition of ABCG2 and Pgp were approximately 1.4 and approximately 3.0 microM, respectively. Because ABC transporters are highly expressed at the blood-brain barrier and on many tumor cells, they contribute significantly to treatment failure of many types of cancer, particularly of those within the neuraxis. In addition to its effect on Hh signaling, the ability of HhAntag691 and related compounds to inhibit two key ABC transporters could contribute to their effectiveness in treating malignancies.

minipress overdose death 2017-12-04

Benign prostatic hypertrophy (BPH) produces symptomatic urethral obstruction in a significant percentage of older men. Since the incidence of BPH is age related, the clinical and economic impact of this disease will continue to progress as average lifespan increases. BPH is associated with growth of both glandular and stromal elements of the prostate gland. Glandular hyperplasia can be partially reversed by withdrawal of androgenic tone with androgen receptor antagonists or steroid-5-alpha-reductase inhibitors. However, the reduction in prostatic size produced by these agents has little effect on the dynamic tone induced by nerve mediated contraction of stromal smooth muscle. This tone is mediated by activation of alpha-adrenoceptors. Therefore the alpha-adrenoceptor antagonists represent a useful pharmacological approach to the treatment of BPH. Studies in isolated strips of human prostate show that either exogenous alpha-adrenoceptor agonists or electrical field stimulation will induce contraction. Studies with selective antagonists such as prazosin show that this response is mediated by the alpha 1-adrenoceptor, even though radioligand binding studies show the presence of alpha 1 and alpha 2 adrenoceptor subtypes in approximately equal density. Following the cloning of multiple alpha 1-adrenoceptors, the contractile response in human prostate has been assigned to the alpha 1A adrenoceptor. However, recent data would suggest a functional role for another subtype, which has not yet been cloned, and designated as alpha 1L based on a relatively low affinity for prazosin. Clinical trials have shown efficacy of a variety of alpha-adrenoceptor antagonists in BPH, including non-selective agents such as phenoxybenzamine, as well as a variety of selective alpha 1-adrenoceptor antagonists, most structurally related to prazosin. The agents most commonly employed at the present time include the prazosin analogs terazosin, doxazosin and alfuzosin, as well as the Altace Reviews structurally unrelated indoramin and tamsulosin. The design of new alpha 1-antagonists for BPH has concentrated on agents producing preferential blockage of urogenital vis-á-vis vascular alpha 1-adrenoceptors, based either on selectivity for the alpha 1A-adrenoceptor subtype or on functional uroselectivity in animal models. While these newer agents offer the prospect of reducing the incidence of the cardiovascular side effects associated with current therapy their superiority over nonselective alpha 1-adrenoceptor antagonists remains to be demonstrated in the clinical setting.

minipress xl tablets 2017-04-30

Alpha 1 adrenoceptor binding sites have been characterized in prostatic tissue homogenates using radioligand receptor binding studies. The Desyrel Cost objective of the present study was to characterize and localize prostatic alpha 1 adrenoceptor binding sites using slide-mounted tissue sections and the ligand 3H-prazosin. The present study demonstrated that preincubation is not required; the optimal incubation interval is 40 minutes; and a 1-minute wash (once or twice) maximizes the proportion of specific 3H-prazosin binding. Saturation studies were performed at 8 different concentrations of 3H-prazosin ranging between 0.0625 nM. to 8.0 nM. The binding of 3H-prazosin was consistently saturable and of high affinity. The mean Kd and Bmax determined from 6 saturation studies was 4.16 x 10(-10) M. and 1.30 fmol./mg. wet weight, respectively. The pharmacology of these 3H-prazosin binding sites was characterized using competitive displacement experiments. The mean IC50 corrected for prazosin, phentolamine and yohimbine was 7.8 x 10(-10) M., 6.0 x 10(-9) M. and 2.1 x 10(-6) M. The rank order of the IC50 corrected values indicates that alpha 1 binding sites were measured under the assay conditions. In the present study, the mean values for Kd, Bmax and IC50 corrected are similar to values previously reported using prostatic tissue homogenates. Prostatic tissue sections were apposed to x-ray film after being incubated with 3 nM. 3H-prazosin (total prazosin binding) and 3 nM. 3H-prazosin + 8 microM. prazosin (nonspecific prazosin binding). The autoradiograms were analyzed using a computerized analyzing system. The specific radioactive densities of 3H-prazosin in the stroma and glandular epithelium were 1099 +/- 48 pCi/mg. and 163 +/- 42 pCi/mg. The present study validates the technique of assaying alpha 1 adrenoceptor binding sites on slide-mounted prostatic tissue sections and provides further evidence that alpha 1 adrenoceptor binding sites are localized primarily to the stromal elements of the prostate.

minipress pill 2015-01-28

In the rat muscle vascular bed, vasoconstrictors either increase or decrease oxygen consumption (VO2). The present study compared the effects of norepinephrine (NE), angiotensin II (ANG II), and 5-hydroxytryptamine (5-HT) on vasoconstriction-associated metabolism in the constant-flow perfused hindlimb of spontaneously hypertensive rats (SHR) and Wistar Nizoral Cream Dosage -Kyoto rats (WKY) in the absence of insulin. Basal perfusion pressure, VO2, glucose uptake, and lactate production were increased by 21.4, 11.9, 46.4, and 44.9% (P < 0.05 for all), respectively, in SHR, which also had higher blood pressure and metabolic rate (P < 0.05) in vivo. Dose-response curves for NE-induced perfusion pressure, VO2, and lactate production in SHR were shifted to the left compared with WKY. Associated with the increased perfusion pressure, NE-induced VO2 and glucose uptake were both decreased (P < 0.01), particularly at high concentrations. These differences were unaffected by 10 microM propranolol but were all diminished by further addition of prazosin (2.5 nM). ANG II stimulated VO2, glucose uptake, and lactate production in both strains, but the increased lactate production was smaller in SHR (P < 0.05) with a proportional decrease (P < 0.05) in glucose uptake. Conversely, 5-HT decreased VO2 in both strains (P < 0.01), and this effect was greater in SHR (P < 0.01). These data suggest that SHR muscle thermogenesis and glucose uptake are impaired during vasoconstriction, especially in response to NE.

minipress nightmares dosage 2015-08-05

The effects of iontophoretically applied noradrenaline have been tested on intracellularly recorded locus coeruleus neurons grown in explant cultures from neonatal mice. In addition to hyperpolarizing responses mediated by alpha 2-adrenergic receptors, as observed in locus coeruleus neurons in vivo and in brain slices from adult animals, alpha 1-mediated depolarizations were observed to succeed the initial hyperpolarizations in some cultures. It was shown that the depolarizing responses were only present in younger cultures, i.e., less than 26 days in vitro. In cultures less than 20 days old, all cells displayed the biphasic hyperpolarizing-depolarizing responses. Both components of the response appear to be direct, since they were present when synaptic transmission was blocked by including tetrodotoxin or by altering divalent cations in the perfusate. The depolarizing responses were frequently reduced in solutions with altered divalent cation content, and this might reflect a calcium dependency of this response. The hyperpolarizing and depolarizing components of the responses to noradrenaline were progressively blocked by increasing concentrations of the selective antagonists yohimbine and prazosin, respectively, in the dose ranges of 100 mM - 1 microM (yohimbine) and 20-200 nM (prazosin). Recent Imitrex 10 Mg results from electrophysiological studies of locus coeruleus neurons in brain slices suggest that similar changes occur in the animal as well as in culture. It is possible that the transient depolarizing responses reflect a developmentally important enhanced responsiveness of locus coeruleus neurons during the early postnatal period.

minipress cost 2017-11-22

Central nitric oxide (NO) has an important role in hypothermia induced by hypoxia as well as in that elicited by noradrenaline (NA) microinjected into the rostromedial preoptic area (POA) of the hypothalamus. Here, I tested the hypothesis that activation of adrenoceptors and NO in the rostromedial POA is involved in hypoxia-induced hypothermia in urethane-chloralose-anesthetized, neuromuscularly blocked, artificially ventilated rats. Hypoxic ventilation (10% O2-90% N2, 5 min) evoked an increase in the tail skin temperature and a decrease in the colonic temperature, though these changes occurred at 30 s to 7 min after returning the rats to ventilation with room air. These responses were eliminated by prior bilateral transection of the carotid sinus nerves, but not by bilateral cervical vagotomy, suggesting the involvement of activated carotid chemoreceptors in the hypoxic ventilation-induced Cymbalta Capsule hypothermia. Such responses were also greatly attenuated by the microinjection of an NO synthase (NOS) inhibitor, NG-monomethyl-L-arginine (L-NMMA, 25 nmol), but not by that of its inactive enantiomer, NG-monomethyl-D-arginine (D-NMMA, 25 nmol), into the NA-sensitive, hypothermia-inducing site in the rostromedial POA. Pretreatment with the α1-adrenoceptor blocker prazosin (50 pmol), but not vehicle saline, also greatly attenuated the hypoxic ventilation-induced heat loss responses. These results suggest that this hypoxia-induced hypothermia was mediated, at least in part, by activation of α1-adrenoceptors and NOS in the rostromedial POA.

tab minipress dose 2016-08-26

In dog pulmonary arterial and venous strips without endothelium under treatment with prazosin, nicotine induced relaxation that was abolished by N(G)-nitro-L-arginine, hexamethonium and methylene blue. L-Arginine antagonized the N(G)-nitro-L-arginine action. Neurogenic relaxations tended to be more evident in the vein. Nitric oxide (NO)-induced relaxations were greater in the veins than in the arteries. Concentrations of NO to induce the same magnitude of relaxation as that to nicotine were higher in the arteries. In conclusion, dog pulmonary arteries Lamictal 350 Mg and veins are innervated by nitroxidergic (nitrergic) nerves, and NO is released by nerve stimulation with nicotine in a larger amount in the artery than the vein.

minipress user reviews 2015-04-16

To characterize the blood pressure and heart rate effects of atrial natriuretic peptide (ANP) in the brain, we administered 20 micrograms/kg of atriopeptin III in 5 microliters of 0.9 normal saline into the fourth ventricle of awake, freely moving, spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. ANP produced a 13 +/- 1 mmHg decrease in mean arterial blood pressure (MAP) in the SHR (P less than 0.001 vs. base line or saline control, n = 10) and a 9 +/- 2 mmHg decrease in the WKY (P less than 0.02). Heart rate did not change significantly in response to ANP. To determine whether an interaction with the adrenergic nervous system played a role in the effects of ANP, we administered 100 ng yohimbine HCL, an alpha 2-antagonist, by intracerebroventricular injection, 45 min before ANP and completely prevented the ANP-induced decrease in MAP. In contrast, 100 ng intracerebroventricular prazosin, an alpha 1-adrenergic antagonist, had no significant influence on the MAP effect induced by ANP. A third group of SHR was pretreated with intracerebroventricular 6-OH dopamine to deplete central catecholamines or with saline. The rats pretreated with 6-OH dopamine (n = 6) had no significant response to ANP, which was administered 9 days later. This was significantly different from the saline-pretreated control group (n = 6), which responded with a 19 +/- 3 mmHg decrease in MAP (P less than 0.025). These studies indicate that the administration of ANP into the fourth ventricle of the brain decreases the MAP of rats through an interaction with the central alpha 2-adrenergic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

minipress drug information 2017-07-05

Repeated electroconvulsion shock (ECS) for 7 days given to mildly reserpinized rats strongly elevated the density of [3H]prazosin-labelled alpha 1-adrenoceptors and depressed the EC50 for norepinephrine-stimulated inositol phosphate accumulation, while the effects of either treatment given alone were small or negligible. Alterations in alpha 1-adrenoceptor activity caused by ECS could possibly be a function of receptor sensitivity during drug treatment.

minipress tablets 2015-07-18

1. At 30 weeks of age, homozygote diabetic C57 BL KsJ (db/db) mice were grossly obese, lethargic and displayed moderate hair loss relative to heterozygote control C 57 BL KsJ (db/+) mice. 2. In diabetic mice, compared to control, the total body weights, liver weight: body weight ratios, and blood glucose levels were increased 2.3 fold, 20% and 3.1 fold, respectively. 3. Analysis of plasma membranes isolated from control and diabetic mouse liver established that comparable purity levels were achieved since relative specific activities of the plasma membrane markers 5'-nucleotidase and gamma-glutamyltranspeptidase were similar: 10.2 and 11.4 fold with respect to 5'-nucleotidase in control and diabetic states respectively; and 8.0 and 8.3 fold with respect to gamma-glutamyltranspeptidase in control and diabetic states respectively. 4. A select effect of diabetes on gamma-glutamyltranspepetidase, however, was observed. The activity of this enzyme was found to be reduced 16% in diabetic liver compared to control liver. 5. Assessment of [3H]prazosin and [3H]dihydrolalprenolol binding to mouse liver plasma membranes indicated that although there was no difference in beta-adrenergic receptor binding in control and diabetic states, alpha 1-adrenergic receptor binding was found to be reduced 43% in diabetic mouse liver plasma membranes. 6. Scatchard analyses of kinetic studies indicate that the reduction is a reflection of decreases in alpha 1-adrenergic receptor numbers with no change in alpha 1 receptor affinity in the diabetic state: since for diabetic and control liver plasma membranes, Kd values were 3.41 +/- 0.02 nM and 3.40 +/- 0.01 nM respectively; and Bmax were 650.12 +/- 16.44 fmol mg-1 and 380.76 +/- 12.92 fmol mg-1, respectively.

minipress drug 2015-11-12

The anticonvulsant (AC drug)- or ethanol (EtOH)-modified effects of cardiovascular (CV) drugs against cocaine (COCA)-induced toxicity were examined in male ICR mice. Nontoxic doses of the CV drugs nimodipine (NIMO), prazosin (PRA), phentolamine (PHEN), propranolol (PRO), and enalapril (ENA) were used with or without the AC drugs diazepam (DZP), phenobarbital (PHB), phenytoin (PHY), and EtOH. Each CV drug combined with or without each AC drug was administered intraperitoneally (IP) 5 min before an IP injection of COCA 75 mg/kg. Of the CV drugs examined, PRA 5 mg/kg and PHEN 5 mg/kg protected against COCA-induced seizures, but only the alpha1-adrenergic blocking agent PRA protected against COCA-induced deaths. Of the AC drugs examined, DZP 5 mg/kg and PHB 50 mg/kg, as well as EtOH 3 g/kg, attenuated the severity of the COCA-induced seizures, but only PHB protected against COCA-induced deaths. The total mortality rate was significantly, often synergistically, decreased compared to the COCA-only group when the appropriate CV drugs were combined with the AC drugs: PRA 5 mg/kg in the EtOH-cotreated groups, PRA 5 mg/kg, PHEN 5 mg/kg or ENA 10 mg/kg in the DZP-cotreated groups, and NIMO 5 mg/kg, PRA 5 mg/kg, PHEN 5 mg/kg, or PRO 10 mg/kg in the PHB-cotreated groups. The decrease in the COCA concentration in the blood and/or brain was not always accompanied by an attenuation of the mortality rate. However, the attenuation of severe seizures by a single PRA, PHEN, DZP, or PHB cotreatment was accompanied by a decrease in the brain COCA concentration.

minipress max dose 2017-03-20

Contractions of the dorsal pedal artery and saphenous vein to phorbol 12,13-dibutyrate (PDBu), 12-O-tetradecanoylphorbol 13-acetate (TPA), and 4 alpha-phorbol 12,13-didecanoate (4 alpha-phorbol) were measured from dogs with and without pacing-induced heart failure. The effects of polymyxin B (a relatively selective protein kinase C inhibitor), nifedipine (calcium channel blocker), and prazosin (alpha 1-adrenoceptor antagonist) were examined on the contractions developed to PDBu before heart failure, after 1 week of pacing, and at end-stage heart failure. PDBu and TPA, but not 4 alpha-phorbol, produced concentration-dependent increases in contractile force in both the artery and the vein. In the dorsal pedal artery, efficacy of and sensitivity to PDBu and TPA were enhanced after 1 week of pacing, but returned to control level at end-stage heart failure. In the saphenous vein, the concentration-effect curve to PDBu was displaced to the left after 1 week of pacing; EC50 values for PDBu were 3.2 x 10(-9) and 3.2 x 10(-8) M for 1 week paced and control, respectively. Polymyxin B significantly decreased the efficacy of PDBu in the dorsal pedal artery at all time points, but was less effective with advancing heart failure. In contrast, in the vein, there was a significant increase in inhibitory potential at end-stage heart failure. In all cases, nifedipine inhibited PDBu in a concentration-dependent manner. With the progression of heart failure, the contractions of the saphenous vein, developed to PDBu, became more sensitive to inhibition by nifedipine. Prazosin failed to inhibit vascular effects of PDBu. These results are discussed in terms of protein kinase C involvement in vascular contractions and its role in the pathogenesis of heart failure.