The appearance of multiresistant bacterial strains coupled with the globally ongoing problem of infectious diseases point to the imperative need for novel and affordable antimicrobial drugs. The antibacterial potential of cardiovascular non-antibiotics such as amlodipine (AML), dobutamine, lacidipine, nifedipine and oxyfedrine has been reported previously. Of these drugs, AML proved to have the most significant antibacterial activity against Gram-positive and Gram-negative bacteria. Time-kill curve studies indicate that this Ca(2+) channel blocker exhibits bactericidal activity against Listeria monocytogenes and Staphylococcus aureus. AML could protect against murine listeriosis and salmonellosis at doses ranging within its maximum recommended human or non-toxic ex vivo dose. AML acts as a 'helper compound' in synergistic combination with streptomycin against several Gram-positive and Gram-negative bacterial strains in vitro as well as in the murine salmonellosis model in vivo. The present review focuses on the possible use of cardiovascular non-antibiotics such as AML as auxiliary compound targets for synergistic combinations in infections and hypertension conditions, rationalised on the basis of the activities of the compounds.
A case of severe macroglossia and angioedema in a child with Burkitt lymphoma who was treated with two dihydropyridine calcium-channel blockers is reported.
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This study was aimed at investigating the possible relationship between the physical properties and the permeation of S-amlodipine and RS-amlodipine and studying the possible enantioselectivity of permeation of amlodipine in the presence and absence of enhancers, such as terpene enhancers and ethanol.
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Chronic lead exposure is known to be a risk factor for hypertension (HTN). No specific medication is recommended for the treatment of lead-induced hypertension (LIHTN).
The study was aimed to observe the effect of amlodipine on rat pituitary gonadotropins after amlodipine administration and withdrawal.
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After a 2-week placebo period, 300 hypertensive patients with type 2 diabetes and microalbuminuria were treated with the 40 mg of telmisartan and 2.5 mg of amlodipine combination. After 4 weeks 210 patients whose blood pressure (BP) was not controlled (BP >130/80 mm Hg) were randomized to two-dose titration regimens, one based on increasing doses of telmisartan (up to 160 mg daily) and fixed 2.5-mg dose of amlodipine, the other based on increasing doses of amlodipine (up to 10 mg daily) and fixed 40-mg dose of telmisartan. After 12 weeks the nonresponder patients were given transdermic clonidine (0.1mg/d). After 16 weeks the patients yet not controlled were discontinued, the others were followed for 48 weeks. Office BP, UAER, creatinine clearance, plasma potassium, fasting glycemia, and glycosylated hemoglobin were assessed at the end of the telmisartan (40 mg)/amlodipine (2.5 mg) treatment period and after 48 weeks of treatment.
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The dose-dependent (1, 5, 10, 50 microM) antioxidative activity of calcium antagonists (verapamil, diltiazem, nifedipine, amlodipine, isradipine or lacidipine) and alpha-tocopherol against copper-induced LDL (0.25 mg/ml) oxidation was compared by measuring the diene formation and the content of TBARS. For diltiazem no antioxidant effect could be found, whereas the other calcium antagonists and alpha-tocopherol have demonstrated antioxidant activity at least at concentrations of 10 and 50 microM: alpha-tocopherol > lacidipine > nifedipine > isradipine, verapamil, amlodipine. Additionally, alpha-tocopherol and lacidipine were able to attenuate LDL-oxidation significantly at 1 and 5 microM. These results indicate in vitro antioxidative activity of calcium antagonists especially from the dihydropyridine-type with greatest activity for the strongly lipophilic lacidipine. This might be one possible antiatherogenic mechanism of calcium antagonists, since oxidative modification enhances the atherogenic potential of LDL.
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In this review the calcium channel blockers (CCB) were divided into three generations. The advantages and shortcomings of these drugs were described. The application of CCB in the treatment of hypertensive disease, ischaemic heart disease, congestive heart failure and heart arrhythmias was discussed. Actually, the optimal drugs from this group are representatives of the third generation: amlodipine and lacidipine. It seems that search for new CCB should be directed to find the substances similar to or better than the chemical entities of this third generation. The calcium sensitizing agents as a new positive inotropic drugs are signalled. The possibility that in the future the new CCB could have an application as psychotropic drugs is mentioned.
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The influx of calcium in response to vasopressin receptor stimulation is an important component of excitation-contraction coupling. We have examined the routes by which Ca2+ and other divalent cations enter vascular smooth muscle cells using a cultured vascular smooth muscle cell line (A7r5). Confluent A7r5 cells were loaded with Fura-2 to permit measurement of intracellular divalent cation concentration (Ca2+, Ba2+, Mn2+). Combinations of excitation wavelengths (340/380, 340/356, 356/380 and 340/370) were used depending on the divalent cation being studied. Emission was measured at 510 nm for all studies. Ca2+, Ba2+ and Mn2+ permeated unstimulated A7r5 cells. Vasopressin increased intracellular Ca2+ in cells both in the presence and absence of extracellular Ca2+, although responses in the absence of extracellular Ca2+ were smaller and had no sustained component. Amlodipine, a voltage-dependent calcium channel blocker, had no effect on Ca2+ entry, but Ni2+ did block Ca2+ influx. Vasopressin-induced elevations of intracellular Ca2+ in Ca(2+)-free physiological saline were abolished by ionomycin and thapsigargin. In the presence of extracellular Ba2+ vasopressin increased intracellular Ca2+ transiently and caused a small sustained increase in intracellular Ba2+ concentration. Ionomycin and thapsigargin increased intracellular Ca2+ but had no effect on Ba2+ influx. In contrast vasopressin, ionomycin and thapsigargin had no effect on Mn2+ influx. Econazole and SKF 96365, imidazoles reported to be blockers of receptor-induced cation entry, increased intracellular Ca2+ by releasing intracellular Ca2+ from a different site to that mobilized by vasopressin or thapsigargin in A7r5 cells. Econazole and SKF 96365 partially inhibited passive influx of Ca2+ and Ba2+ but did not inhibit passive influx of Mn2+, or vasopressin-induced influx of Ba2+. U73122, a putative inhibitor of phospholipase C partially inhibited passive entry of Ca2+ but not passive entry of Mn2+ and Ba2+. U73122 also inhibited vasopressin-induced release of intracellular Ca2+ and agonist-induced Ca2+ influx but did not block vasopressin-induced Ba2+ influx. Divalent cations enter A7r5 cells by a number of routes - 'passive' pathway(s) that admit Ca2+, Ba2+ and Mn2+ and receptor-operated pathway(s) that are permeable to Ca2+, Ba2+ but not Mn2+. On the basis of ionic permeabilities and the effect of various blocking agents, there appear to be two distinct passive influx routes. One is permeable to Ca2+ and Ba2+ and is blocked by econazole or SKF 96365. The other is permeable to Mn2+ and is blocked by Ni2+. There also appear to be two different routes of divalent cation entry involved in responses to receptor activation.(ABSTRACT TRUNCATED AT 400 WORDS)
Recently it has been recognized that not only blood pressure (BP) but also pulse rate (PR) assessed in the setting of the patient's home by a home BP monitoring device has higher predictive power for cardiovascular events than similar measurements made in the office setting. In this study, we compared the efficacy of azelnidipine to that of amlodipine in lowering morning BP and reducing PR in outpatients with essential hypertension. Patients were assigned to receive once daily administration of azelnidipine 8-16 mg/day (n = 54) or amlodipine 2.5-5 mg/day (n = 54) for 8 weeks. Morning BP and PR were evaluated by assessing patients' self-monitored BP and PR in the home environment. The mean reductions of morning systolic/diastolic BP (SBP/DBP) in the azelnidipine and amlodipine groups were similar (-24.1 +/- 11.8/-14.1 +/- 10.7 vs. -20.4 +/- 11.7/-12.2 +/- 7.7 mmHg). However, whereas azelnidipine decreased mean PR by -6.4 +/- 8.3 beats/min (p < 0.05 vs. baseline), amlodipine did not cause significant reduction of this parameter (-2.1 +/- 8.2 beats/min). Although neither drug changed PR in patients in whom baseline PR was < 70 beats/min, azelnidipine significantly lowered PR in patients whose baseline PR was > 70 beats/min. These results suggest that oral azelnidipine administration may be an effective therapy in the setting of chronic morning hypertension as well as for home PR control.
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There was mild impairment of FMD at baseline (7.3 +/- 0.6%). The change in FMD from baseline was significant only for quinapril (1.8 +/- 1%, p < 0.02). No change was seen with losartan (0.8 +/- 1.1%, p = 0.57), amlodipine (0.3 +/- 0.9%, p = 0.97) or enalapril (-0.2 +/- 0.8%, p = 0.84). No significant change in nitroglycerin-induced dilation occurred with drug therapy. The improvement in quinapril response was not seen in those with the DD ACE genotype (0.5 +/- 2.1%) but was seen in those with the ID and II genotype (3.3 +/- 1.2 and 3.2 +/- 1.9%, respectively, p = 0.03).
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The aim of this study was to comparatively assess the effects of irbesartan and amlodipine monotherapies on left ventricular mass index (LVMI) in patients with mild to moderate untreated hypertension and echocardiographically determined left ventricular hypertrophy (LVH). Sixty hypertensive patients (35 men, 25 women; mean age, 52.8 years +/- 12.6) with diastolic blood pressure (BP) > or = 100 mm Hg were randomized to irbesartan 150 mg once daily or amlodipine 5 mg once daily for a 4-week titration period. Dosage of both drugs was increased to irbesartan 300 mg once daily or amlodipine 10 mg once daily in case of sitting diastolic BP still >90 mm Hg after the first 2 weeks of treatment. Dosage doubling was necessary in more than 50% of patients in both treatment groups. After the titration period, only the responders (sitting diastolic BP < or = 90 mm Hg) entered a 5-month maintenance period. After 3 months, echocardiographically estimated LVMI decreased by 23.2% in the irbesartan-treated patients and 11.4% in the amlodipine-treated patients, with an adjusted mean difference of 11.8% in favor of irbesartan (P < 0.0001). After 6 months, it decreased by 24.7% in the irbesartan-treated patients and 13.0% in the amlodipine-treated patients, with an adjusted mean difference of 11.6% in favor of irbesartan (P < 0.0001).
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All the periodontal parameters were statistically highly significant (P = 0.00) amongst H, E and L groups and between responders and non-responders. Statistically highly significant Pearson correlation coefficients were found between mean PPD and mean hyperplastic score, mean CAL and mean hyperplastic score and mean calculus and mean hyperplastic score.
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A liquid chromatography-tandem mass spectrometry (LC-MS/MS) analytical method was developed for quantification of amlodipine in rat plasma. The accuracy, precision, linearity, selectivity and recovery were all within an acceptable range. Male Sprague-Dawley rats were randomly assigned to two groups: amlodipine group and amlodipine + GLT group. Plasma concentrations of amlodipine were determined at the designated time points after oral administration by using the developed LC-MS/MS method, and the main pharmacokinetic parameters were calculated and compared. As ginkgolides A, ginkgolides B, bilobalide, quercetin and kaempferol were the main components of GLT, the effects of these ingredients in GLT on metabolism of amlodipine were further investigated in rat liver microsomes.
Twenty-six patients received amlodipine 5 mg daily for de novo hypertension (group A), and another 10 patients received amlodipine for exacerbation of previously existing hypertension (group B). Hypertension was controlled within 7 days under amlodipine in 23/26 (88.5%, 95%CI: 76.2-100) patients in group A, and 8/10 (80%, 95%CI: 55.2-100) patients in group B, with a favourable toxicity profile.
Hypertension frequently coexists with diabetes mellitus, resulting in increased cardiovascular risk. Thus, BP control is crucial in decreasing morbidity and mortality in this difficult-to-treat patient population.
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The results were analyzed by Student's 't' test The reduction in the average systolic and diastolic blood pressure, in the standing, supine and sitting postures in the S-Amlodipine group as well as in the Amlodipine group after six weeks of treatment was highly significant (P < or = 0.0001). The baseline values for average systolic blood pressure in standing, supine and sitting positions in the S-Amlodipine 2.5 mg treatment group were found to be 164.12 +/- 10.28, 165.72 +/- 10.88 and 165.24 +/- 10.66 mm of Hg respectively, which after treatment of six weeks changed to 144.9 +/- 7.4, 146.04 +/- 8.56 and 145.36 +/- 8.32 mm of Hg. The baseline values for average systolic blood pressure in standing, supine and sitting positions in the Amlodipine 5 mg treatment group were found to be 164.57 +/- 10.36, 166.47 +/- 10.58 and 165.81 +/- 10.54 mm of Hg respectively, which after treatment of six weeks changed to 154.42 +/- 6.33, 147.23 +/- 7.11 and 146.57 +/- 7.54 mm of Hg. The baseline values for average diastolic blood pressure in standing, supine and sitting positions in the S-Amlodipine 2.5 mg treatment group were found to be 99.63 +/- 6.22, 101.13 +/- 7.18 and 100.59 +/- 6.6 mm of Hg respectively, which after treatment of six weeks changed to 86.0 +/- 4.70, 87.18 +/- 5.20 and 86.27 +/- 5.68 mm of Hg. While the baseline values for average diastolic blood pressure in standing, supine and sitting positions in the Amlodipine 5 mg treatment group were found to be 98.95 +/- 5.54, 100.86 +/- 6.71 and 100.38 +/- 6.38 mm of Hg respectively, which after treatment of six weeks changed to 86.19 +/- 4.77, 87.52 +/- 5.44 and 87.33 +/- 5.98 mm of Hg. However the difference in the average reduction in systolic and diastolic blood pressures, in the two treatment groups, in the sitting, supine and the standing positions was not found to be statistically significant (p > 0.1) (CI = 0.95). There was no statistically significant change in the levels of serum creatinine, SGOT, SGPT, HDL, LDL, triglyceride and total cholesterol in patients receiving Amlodipine 5 mg. The reduction in total cholesterol as well as triglyceride level in the S-Amlodipine 2.5 mg treatment group was found to be greater but it failed to show any statistically significant difference.
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Trends were seen during amlodipine treatment towards larger improvements, in serum creatinine (by 8% of baseline on amlodipine vs 4% on nifedipine), lithium clearance (13% vs 2%), and glomerular filtration rate 11% vs 7%). Effective renal plasma flow was increased by 11% of baseline on nifedipine vs 9% on amlodipine. There were no significant differences between treatments. Amlodipine and nifedipine lowered systolic blood pressure to a similar extent (21 mmHg vs 15 mmHg respectively, P=0.25), but amlodipine was more effective than nifedipine in lowering diastolic blood pressure (13 mmHg vs 8 mmHg, P=0.006). Both treatments were well tolerated.
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All patients who were enrolled in the CAMELOT study were included in this economic substudy. Patients with CAD and normal blood pressure were randomized to amlodipine, enalapril or placebo, and followed up for 24 months (between 1999 and 2004). Data on hospitalizations and medication use were obtained from the clinical trial. Costs were assigned from secondary sources. Total costs ($US, year 2004 values) were estimated as the sum of costs associated with cardiovascular hospitalizations, study medications and concomitant cardiovascular medications. Costs and resource use were analysed by treatment arm overall and for selected patient subgroups. Cost differences were evaluated using nonparametric bootstrap techniques.
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Dahl salt-sensitive rats fed a high-salt diet from 6 weeks of age were treated with vehicle (LVH group), amlodipine (3 mg/kg per day), or cilnidipine (3 mg/kg per day) from 7 to 11 weeks.
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Single-pill combination (SPC) therapy of two drugs is recommended by international guidelines, including the Chinese guidelines (2010), for the treatment of hypertension in high-risk patients who require marked blood pressure (BP) reductions. Real-world data on the efficacy and safety of valsartan/amlodipine (Val/Aml) SPC are scarce. The present study is the first observational study in China to evaluate the efficacy (primary endpoint) and safety of Val/Aml (80/5 mg) SPC in Chinese patients with hypertension whose BP was not adequately controlled by monotherapy in a real-world setting.
The value of octreotide scanning in the localization of extra-adrenal pheochromocytoma.Control of catecholamine secretion using high-dose octreotide.This is a report of a rare cause of secondary diabetes and hypertension.
During the 3 months of amlodipine monotherapy, large and small AC were improved by 26% and 38%, respectively, and the systemic vascular resistance was reduced by 10%. The addition of atorvastatin during the next 3 months improved small AC by an additional 42% and decreased the systemic vascular resistance by another 5%, but large AC and blood pressure did not change.
Myocardial oxygen consumption was measured polarographically using a Clark-type oxygen electrode in isolated left ventricular myocardium from 26 explanted failing human hearts obtained at the time of heart transplantation.
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Reducing blood pressure (BP) to target levels is a major priority in preventing clinical events in hypertension. Typically this requires more than one drug, and recent guidelines on hypertension management therefore recommend starting with combination treatment in many patients. Diuretics have often been part of such therapy, usually paired with angiotensin converting enzyme (ACE) inhibitors or similar agents; but calcium channel blockers are also highly efficacious in reducing BP when combined with ACE inhibitors. In addition, these drug classes, separately and in combination, appear to have vasculoprotective properties. Because the primary goal of treating hypertension is to enhance survival and reduce cardiovascular outcomes, the Rationale and Design of Avoiding Cardiovascular events through COMbination therapy in Patients LIving with Systolic Hypertension (ACCOMPLISH) trial is designed as the first blinded and randomized study to prospectively compare the effects on these endpoints of two antihypertensive combinations, benazapril/hydrochlorothiazide (force titrated to 40/12.5 mg) and amlodipine besylate/benazapril (force titrated to 5/40 mg). The doses can be further titrated to 40/25 mg or 10/40 mg, and other classes of drugs can be added as needed for optimal BP control. The primary study endpoint is a composite of cardiovascular mortality and morbidity. The study will be performed in hypertensive patients (systolic BP > or = 160 mm Hg or currently on antihypertensive therapy) with risk factors for cardiovascular events (prior events, target organ damage, kidney disease, or diabetes). A total of 6300 subjects will be randomized to each group with the expectation that a total of 1642 primary endpoints will occur during a 5-year period, providing 90% power to detect the 15% relative reduction in events (alpha = 0.05) hypothesized to favor the amlodipine besylate/benazapril group. The ACCOMPLISH study will be performed in the United States and Europe. The first patient was randomizedduring 2003, and the trial should conclude in 2008.
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A sensitive, specific liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was established for the quantitative determination of amlodipine and bisoprolol, using clenbuterol as the internal standard (IS). The analytes and IS were isolated from 100μL plasma samples by a simple liquid-liquid extraction (LLE). Reverse-phase high performance liquid chromatography (RP-HPLC) separation was accomplished on a Diamonsil C(18) column (50mm×4.6mm, 5μm) with a mobile phase composed of methanol-water-formic acid (75:25:0.01, v/v/v) at a flow rate of 0.3mL/min. The method had a chromatographic total run time of 3min. Multiple reacting monitoring (MRM) transitions of m/z [M+H](+) 409.1→237.9 (amlodipine), m/z [M+H](+) 326.2→116.0 (bisoprolol) and m/z [M+H](+) 277.0→203.0 (clenbuterol, IS) were used to quantify amlodipine, bisoprolol and IS, respectively. The method was sensitive with a lower limit of quantitation (LLOQ) of 0.2ng/mL for both amlodipine and bisoprolol, and the linear range was 0.2-50ng/mL for both amlodipine and bisoprolol (r(2)>0.9961). All the validation data, such as accuracy, precision and inter-day repeatability, were within the required limits. The method was successfully applied to pharmacokinetic studies of amlodipine and bisoprolol in Sprague-Dawley (SD) rats.
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Dihydropyridine calcium antagonists used in this trial seem useful in hypertension because they decrease oxidative stress, and normalize of pressure values.
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A total of 454 hypertensive patients (diabetes and renal insufficiency excluded) were randomized, 227 to each group (56% were men, mean age was 55 years, blood pressure 162.3/101.1 mmHg). After 1 month, superior SBP (-3.1 mmHg, P = 0.02) and DBP (-2.8 mmHg, P < 0.001) reductions were observed with perindopril/indapamide/amlodipine, which were even more pronounced after excluding white-coat effect in the sustained hypertension population (-5.3/-3.7 mmHg). Similar results were observed in terms of blood pressure response (72 vs. 53%, P < 0.0001) and control rates (32 vs. 25%, P = 0.005). Up-titration was effective at each visit in both treatment arms (P < 0.001). Both ABPM and HBPM results confirmed the superiority of the triple therapy at 1 month on ASBP/ADBP and HSBP/HDBP: -4.5/-2.0 mmHg for ABPM (P < 0.001/P = 0.04), and -4.9/-3.1 mmHg for HBPM (both, P < 0.001). Up-titration steps resulted in further significant decreases in both ABPM and HBPM. Both treatment regimens were well tolerated regarding adverse events or laboratory testing. In particular, peripheral edema known to be amlodipine dose dependent, appeared in only a few cases, none with the highest dose. Hypotension, orthostatic hypotension, and cough whatever the dose were infrequent. There were no treatment-related serious adverse events.
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Visceral fat obesity plays an essential role in the clustering of atherosclerotic multiple risk factors in the metabolic syndrome. Telmisartan, an angiotensin II type 1 receptor blocker, has partial agonistic properties for peroxisome proliferator-activated receptor gamma, which is a key regulator of adipocyte differentiation and function.