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Blood pressure decreased equally in all groups. Among patients with comparable BP values on monotherapy, only quinapril-treated patients showed a significant decrease in PWV, aldosterone, and PICP as compared with baseline values. Multiple regression analysis showed that PWV was significantly affected by: age (beta = 0.36; P =.021), systolic BP (beta = 0.45; P =.014), and PICP (beta = 0.27; P =.038).
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Objective To compare 1-year treatment adherence of ramipril + amlodipine and ramipril +hydroclorothiazide fixed-dose combination therapies in patients with hypertension. Methods Data were extracted from the database of the National Health Insurance Fund of Hungary. Treatment adherence was modelled using survival analysis. Results At 2 months after initiation of treatment, 42% of patients using ramipril +hydrochlorothiazide ( n = 28,800) had discontinued treatment, compared with 0% of patients using ramipril + amlodipine ( n = 10,295). At 1 year, treatment adherence was 29% in the ramipril + hydrochlorothiazide group and 54% in the ramipril + amlodipine group. The hazard ratio for discontinuing ramipril + hydrochlorothiazide vs ramipril + amlodipine was 2.318 (95% confidence intervals 2.246, 2.392). Conclusion Ramipril + amlodipine had significantly higher 1-year treatment adherence than ramipril + hydrochlorothiazide in patients with hypertension.
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The mechanism of action of the anti-apoptotic oncogene Bcl-2 and Ca2+ regulation in ischemia-reperfusion injury is still obscure. In this present study, we investigated mitochondrial Ca2+ overloads and mechanism of action of Bcl-2. Eighteen Wistar rats were divided into sham-operated control group (I) (n = 6), ischemia and reperfusion group (II) (n = 6), and amlodipine-treated group (1 mg kg(-1) body weight/daily by oral route for 7 days before inducing ischemia-reperfusion maneuver) (III) (n = 6). Rats were subjected to 1 h of hepatic ischemia followed by 3-h reperfusion. Mitochondrial Ca2+ content was determined and damage was confirmed by transmission electron microscopy. Decrease of mitochondrial Ca2+ level is related to reduction of apoptosis and cellular changes, viz. increased Bcl-2 expression followed by reduction in secondary endoplasmic reticulum, whereas ischemia/reperfusion group shows overloading Ca2+ ions and decrease in Bcl-2 expression as compared to sham-operated rats. Thus, Bcl-2-dependent reduction of Ca2+ is an important component of the anti-apoptotic program in ischemia-reperfusion injury.
Drug induced gingival hyperplasia is an uncommon entity. Anticonvulsants, immunosuppressants and calcium channel blockers are often implicated. We report a case of a 52-year old male who developed amlodipine induced gingival hyperplasia. The etiology and treatment modalities are discussed.
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Previously we found that hypertension potentiates the risk the cataractogenesis. In the present study, we investigated the protective effects of magnesium taurate (MgT) on hypertension and associated lenticular damages against cadmium chloride (CdCl2)-induced hypertensive animals. Male Sprague-Dawley albino rats (150-180g) were assigned to five experimental groups (n=6). Among the five groups, normal group received 0.3% carboxymethyl cellulose (10ml/kg/day, p.o.). Hypertension control group received CdCl2 (0.5mg/kg/day, i.p.). Tests and standard groups received MgT (3 and 6mg/kg/day, p.o.) and amlodipine (3mg/kg/day, p.o.) concurrently with CdCl2 respectively, for six consecutive weeks. Blood pressure, heart rate, and eyes were examined biweekly, and pathophysiological parameters in serum and eye lenses were evaluated after six weeks of the experimental protocol. The chronic administration of MgT concurrently with CdCl2 significantly restored the blood pressure, serum and lens antioxidants (CAT, SOD, GPx, and GSH), MDA level, and ions (Na(+), K(+), and Ca(2+)). Additionally, MgT treatment led to significant increase in the lens proteins (total and soluble), Ca(2+) ATPase, and Na(+)K(+) ATPase activity as compared to hypertension control group. Ophthalmoscope observations indicated that MgT treatments delayed the progression of cataract against the hypertensive state. The study shows that MgT prevents the progression of cataractogenesis via restoration of blood pressure, lenticular oxidative damages, and lens ATPase functions in the hypertensive state. The results suggest that MgT supplement may play a beneficial role to manage hypertension and associated cataractogenesis.
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Amlodipine was not initially suspected as a cause of these symptoms because these effects are not commonly associated with amlodipine therapy. However, due to the temporal relationship and progression of symptoms with increasing amlodipine dosage, drug-related causes were eventually explored. Review of the medical literature suggests myalgias and arthralgias may be adverse effects common to dihydropyridine calcium-channel antagonists.
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Amlodipin and diltiazem of prolonged action have pronounced antianginal effect, diltiazem being more effective and less toxic.
An open-label, two-stage, longitudinal study was employed.
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The purpose of the present study was to investigate whether treatment of male rats with the calcium antagonist amlodipine, used in the treatment of hypertension and angina, interferes with the reproductive function of male rats. Amlodipine treatment (0.04 mg amlodipine besylate/rat/day for 30 days) decreased plasma follicle-stimulating hormone and testosterone but not luteinizing hormone or prolactin concentrations (measured by double-antibody radioimmuno-assay). A significant reduction (23%) was observed in sperm density (sperm suspension collected from the cauda epididymidis) as well as in the amount of mature spermatids (14%) and Sertoli cells (9%) counted in seminiferous tubule cross-sections (400 x magnification). The results reveal the deleterious effects of subacute amlodipine treatment on the reproductive function of male rats.
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"Stunned myocardium" is defined as the prolonged but transient contractile dysfunction of viable myocardium salvaged by reperfusion. For example, a brief 15-min episode of coronary artery occlusion does not result in myocyte necrosis, yet contractile function of the previously ischemic tissue remains profoundly depressed at 0-30% of baseline values for hours to days following reflow. This phenomenon, first characterized in the experimental canine model, has more recently been documented in clinical instances of angina, following cardiac surgery, after angioplasty, and following successful reperfusion for the treatment of acute myocardial infarction. Considerable evidence indicates that calcium antagonists administered prior to coronary occlusion attenuate postischemic stunning in the canine model: verapamil, diltiazem, and amlodipine have been shown to restore contractile function to 50-100% of baseline values during the initial hours following relief of ischemia. Furthermore, both verapamil and nifedipine improved systolic contraction of stunned myocardium even when treatment was "delayed"--i.e., when the agents were administered 30 min after reflow had been established. This improved recovery of contractile function associated with calcium antagonist treatment may be due in part to the well-documented afterload reducing and coronary vasodilatory properties of these agents. However, as low doses of intracoronary nifedipine infused after reperfusion restored systolic contraction to 75-90% of baseline values in the absence of afterload reduction or increases in coronary blood flow, these data suggest that calcium antagonists may act in part by favorably modulating calcium flux within the stunned, previously ischemic myocytes.(ABSTRACT TRUNCATED AT 250 WORDS)
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Clinical studies have found that the antihypertensive effects of mibefradil are comparable with those of nifedipine, verapamil, and amlodipine, and more effective than those of diltiazem. These effects result from peripheral vasodilation and a slight reduction in heart rate. Selective vasodilation of the coronary vasculature makes it an effective antianginal agent when used alone or added to beta-blocker therapy. Mibefradil demonstrates no significant effects on cardiac contractility, and no adrenergic stimulation resulting in reflex tachycardia. Therefore, it may have some advantages over currently available CCAs, especially in patients with congestive heart failure, although such advantages are unproven in published clinical trials. Ongoing clinical studies, including the Mortality Assessment in Congestive Heart Failure Trial (MACH-1) currently in progress, are needed to clarify mibefradil's place in cardiovascular therapy.
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Calcium channel blockers (CCBs) are prescribed to patients with Marfan syndrome for prophylaxis against aortic aneurysm progression, despite limited evidence for their efficacy and safety in the disorder. Unexpectedly, Marfan mice treated with CCBs show accelerated aneurysm expansion, rupture, and premature lethality. This effect is both extracellular signal-regulated kinase (ERK1/2) dependent and angiotensin-II type 1 receptor (AT1R) dependent. We have identified protein kinase C beta (PKCβ) as a critical mediator of this pathway and demonstrate that the PKCβ inhibitor enzastaurin, and the clinically available anti-hypertensive agent hydralazine, both normalize aortic growth in Marfan mice, in association with reduced PKCβ and ERK1/2 activation. Furthermore, patients with Marfan syndrome and other forms of inherited thoracic aortic aneurysm taking CCBs display increased risk of aortic dissection and need for aortic surgery, compared to patients on other antihypertensive agents.
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Heart rate variability (HRV) was assessed before and after 12-16 weeks of treatment with calcium antagonists in 89 patients with mild and moderate hypertension.
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Test and reference formulations gave a mean Cmax of 5.234±0.914 ng/mL and 4.991±0.563 ng/mL, 108.839±13.601 ng/mL and 114.783±12.315 ng/mL and 97.814±10.779 ng/mL and 93.731±10.018 ng/mL for amlodipine, telmisartan and hydrochlorothiazide respectively. The AUC0-t of amlodipine, telmisartan and hydrochlorothiazide was 161.484 ng.h/mL, 1 917.644 ng.h/mL and 822.847 ng.h/mL for test formulation and 162.108 ng.h/mL, 2 014.764 ng.h/mL and 829.323 ng.h/mL for reference in the fasting state.
In normal pregnancy ET-1,2 content was low while urine NO metabolites levels were high. This contributes to maintaining adequate reaction of the brachial artery in response to the "shiftstress". In women with edema the brachial artery response to short-term occlusion was decreased. In women with both high blood pressure and edema had vascular response paradoxically spastic with a two-fold decrease in blood flow rate, high plasma ET-1.2 contents and low urine NO metabolites levels. Normodipine in gestational arterial hypertension normalizes both blood pressure and EDVD.
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A novel series of diblock copolymers, poly(butyl methacrylate)(n) -block-poly(glycidyl methacrylate)(m) [P(BMA)(n) -b-P(GMA)(m) ], were synthesized by atom transfer radical polymerization and developed as covalent coating of capillaries. The excellent performance of this coating in separation of three 1,4-dihydropyridines (DHPs) derivatives (amlodipine, nicardipine, nitrendipine) was achieved when the diblock copolymers self-assembled into micelles, which was confirmed by transmission electron microscopy, dynamic light scattering, and atom force microscopy. Meanwhile, the effects of block ratio n/m, pH value, buffer concentration, and organic solvents on the separation of 1,4-DHPs were investigated in detail. Then, the relationship between the morphologies of copolymers and the separation resolutions of 1,4-DHPs was discussed. Furthermore, the proposed method exhibited good run-to-run and column-to-column precision with relative standard deviations of electroosmotic flow less than 3.0%. It was also validated with linearity of three 1,4-DHPs in the range of 0.01-1.80 mM (r(2) ≥ 99.7%), efficient recovery (94-103%), and good repeatability (≤ 3.8%). In addition, three 1,4-DHPs were successfully separated in the spiked human serum sample, which indicated the potential utility of this method in biological sample analysis.
ABSTRACT (ARB), in essential hypertensive patients not adequately controlled by amlodipine monotherapy.
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The calcium channel blockers have individual pharmacological and therapeutic properties that may vary, but as a group, they are effective antihypertensive agents in patients with renal disease. Their effects on the kidney may extend beyond BP reduction alone. Fifteen one-year-old male spontaneously hypertensive rats (SHR) were separated in three groups: Initial control group (IC), Final control group (FC, SHR received standard rat chow and fresh water ad libitum during 15 weeks), Amlodipine group (Aml, SHR) received 0.2 mg/kg/day of amlodipine in addition to food and water during 15 weeks. The glomerular number was estimated using the disector method. In the Control group, the BP level increased almost 20 per cent in the first six weeks (from 186 +/- 11 to 223 +/- 16 mmHg, p<0.01) and then BP level increased almost 15 percent until week 15 (from 223 +/- 16 to 258 +/- 20 mmHg, p<0.01). In the same period, the Aml group showed a progressively low BP, reaching a level almost 50 per cent lower in the week 15 than in the week 1 (from 190 +/- 15 to 101+/-8 mmHg, p<0.01). Amlodipine treatment significantly decreased the serum creatinine, more than 12 per cent lower than the FC group (from 70.4 +/- 6.2 to 61.4 +/- 5.2 micromol/L, p<0.05). However, proteinuria was not different when groups were compared. The FC group reached a glomerular number almost 20 percent smaller than the IC and Aml groups (from 35 x 10(3) +/- 7 x 10(3) in IC group, 34 x 10(3) +/- 4 x 10(3) in Aml group to 27 x 10(3) +/- 3 x 10(3) in FC group, p<0.05). A possible protective effect of amlodipine against the loss of glomeruli in SHR is a major additional action of amlodipine in the treatment of hypertension mainly when the renal lesion already exists.
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Angiotensin II (Ang II) has been linked to vascular dysfunction and target-organ damage. Blockade of the angiotensin II type 1 receptor (AT(1)) with an angiotensin receptor blocker may reverse vascular pathology independent of blood pressure (BP) lowering. Stage I hypertensive, nondiabetic patients (61% male; age 38 to 67 years) were randomized after a 4-week washout period to olmesartan medoxomil 20 to 40 mg or atenolol 50 to 100 mg plus additional agents (hydrochlorothiazide, amlodipine, or hydralazine) as needed for a goal BP <140/90 mm Hg. At baseline and after 1 year of treatment, subcutaneous gluteal resistance arteries were examined on a pressurized myograph to evaluate remodeling. Biopsies were available from 22 atenolol recipients, 27 olmesartan medoxomil recipients, and 11 normal volunteer controls. BP was reduced to a comparable degree by olmesartan medoxomil (from 149 +/- 11/92 +/- 8 mm Hg to 120 +/- 9/77 +/- 6 mm Hg; P < .05 [mean +/- standard deviation]) and atenolol (from 147 +/- 10/90 +/- 6 mm Hg to 125 +/- 12/78 +/- 7 mm Hg; P < .05 [mean +/- standard deviation]) from baseline for each arm (P = .08 for the 40-week treatment mean between arms). After one year's treatment, the wall-to-lumen ratio in arteries from patients treated with olmesartan medoxomil was significantly reduced (from 14.9% to 11.1%; P < .01), whereas no significant change was observed in arteries from atenolol-treated patients (from 16.0% to 15.5%; P = NS); the wall-to-lumen ratio in controls was 11.0%. Blockade of AT(1) receptors showed a superior corrective effect on the altered structure of resistance arteries in essential hypertension that was independent of the magnitude of BP reduction, and resulted in values similar to those in normotensive controls.
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Calcium channel blockers such as amlodipine are effective antihypertensive agents. In this study we investigated the effects of amlodipine on vascular oxidative stress, expression of the lectin-like oxidized low-density lipoprotein receptor (LOX-1), and endothelial function in angiotensin (Ang) II-infused rats.