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Amlodipine/valsartan 5/160 mg SPC is a safe and effective therapy for lowering BP in predominantly Chinese adults with stage 1 or 2 hypertension not adequately controlled with valsartan 160 mg monotherapy.
We have investigated the effect of intracellular calcium levels for membrane potential during noradrenaline application in isolated small arteries. Rat mesenteric small arteries were mounted for isometric tension measurement. Smooth muscle membrane potentials were measured by conventional intracellular electrodes, and intracellular calcium concentration was measured using Fura-2 fluorescence. Under control conditions, noradrenaline caused contraction and depolarization from -55.5 to -29.3 mV. In intact arteries, depleting intracellular calcium stores with thapsigargin caused smooth muscle hyperpolarization and inhibited contraction to noradrenaline. In de-endothelialized vessels, thapsigargin still depleted calcium stores, but did not affect either the depolarization or contraction caused by noradrenaline. In noradrenaline-activated vessels, inhibition of calcium influx by amlodipine caused tension and calcium levels to fall to near-baseline levels, but membrane potential returned by only 55%. Treatment with a combination of thapsigargin, D-600 and BAPTA-AM inhibited the tension and calcium responses to noradrenaline, but the membrane potential response was reduced by only 34%. Acute reduction of extracellular chloride concentration caused similar, small depolarization at rest and during noradrenaline exposure. It is concluded that an elevation of intracellular calcium concentration is not essential for noradrenaline depolarization, although part of the depolarization is associated with the raised intracellular calcium level.
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Eight weeks of amlodipine treatment significantly reduced the levels of total cholesterol, low-density lipoprotein cholesterol and triglycerides in the group on the hypercholesterolaemic diet (p < 0.05). In the blood, the level of thiobarbituric acid-reactive substances increased in the rabbits on the 2% cholesterol diet (group 2) and 2% cholesterol-plusamlodipine diet (group 4) and decreased in the amlodipineonly group (group 3) (p < 0.05). Lipid peroxidation in the heart tissue was similar to that in the blood, except in the amlodipine-only group (group 3). In the blood, the activity of total SOD (tSOD) decreased in the group on the 2% cholesterol diet (group 2) (p < 0.05) and markedly increased in the amlodipine-only (group 3) and 2% cholesterol-plusamlodipine groups (group 4) (p < 0.05).
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After a lead-in period with amlodipine monotherapy, 812 non-responder patients (mean sitting diastolic BP > or =95 mmHg) were randomized to one of three treatment groups. Ambulatory BP monitoring was conducted in 276 patients.
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In a multicenter, double-blind, parallel study 828 elderly (aged > or =60 years) hypertensives were randomized to lercanidipine 10 mg/day (n = 420), amlodipine 5 mg/day (n = 200), or lacidipine 2 mg/day (n = 208) (ratio 2:1:1). If blood pressure (BP) control was unsatisfactory (systolic BP/diastolic BP > or =140/90 mm Hg), the dose of the double-blind medication was doubled and, as a further step, enalapril or atenolol (plus diuretic, if needed) was added. Patients were treated for an average of 12 months.
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The objective of this study was to investigate the effects of a single pill of amlodipine (5 mg)/atorvastatin (10 mg) on oxidative stress, blood pressure/lipid control and adherence to medication in patients with type 2 diabetes.
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Although end-stage renal disease (ESRD) currently affects only a small percentage (<0.2%) of the US population, its precursor, the mild and moderate forms of chronic kidney disease (CKD), affects 11% of the population, with significant growth in both ESRD and CKD anticipated in the rapidly aging US population. The primary diagnoses in the majority of ESRD patients are diabetes and hypertension. Results of clinical studies demonstrate that the level of proteinuria and sympathetic activation contribute to the progression of CKD to ESRD. There are sufficient clinical data to demonstrate that the dihydropyridine calcium channel blocker (DHP CCB) class of antihypertensives such as amlodipine and nifedipine, although effective in reducing systemic hypertension, lack activity in reducing proteinuria or attenuating sympathetic activity. Experimental studies and a limited number of clinical studies suggest that non-DHP CCBs, including verapamil and diltiazem, have a mechanism of action that differs from DHP CCBs. Non-DHP CCBs could potentially attenuate sympathetic activity and reduce protein excretion in patients with CKD.
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Angiotensin-converting enzyme inhibitors (ACEI) have a well-established role in the prevention of cardiovascular events in hypertension, left ventricular dysfunction, and heart failure. More recently, ACEI have been shown to prevent cardiovascular events in individuals with increased cardiovascular risk, where hypertension, left ventricular dysfunction, or heart failure was not the primary indication for ACEI therapy.
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Central pressures were derived from brachial pressure and radial pulse wave analysis in 2,073 patients, and 7,146 measurements were recorded and analyzed over follow-up for up to 4 years.
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A sample of 9995 high-risk, non-diabetic hypertensive patients.
In 2010, the American College of Medical Toxicology (ACMT) established its Case Registry, the Toxicology Investigators Consortium (ToxIC). All cases are entered prospectively and include only suspected and confirmed toxic exposures cared for at the bedside by board-certified or board-eligible medical toxicologists at its participating sites. The primary aims of establishing this Registry include the development of a realtime toxico-surveillance system in order to identify and describe current or evolving trends in poisoning and to develop a research tool in toxicology. ToxIC allows for extraction of data from medical records from multiple sites across a national and international network. All cases seen by medical toxicologists at participating institutions were entered into the database. Information characterizing patients entered in 2012 was tabulated and data from the previous years including 2010 and 2011 were included so that cumulative numbers and trends could be described as well. The current report includes data through December 31st, 2012. During 2012, 38 sites with 68 specific institutions contributed a total of 7,269 cases to the Registry. The total number of cases entered into the Registry at the end of 2012 was 17,681. Emergency departments remained the most common source of consultation in 2012, accounting for 61 % of cases. The most common reason for consultation was for pharmaceutical overdose, which occurred in 52 % of patients including intentional (41 %) and unintentional (11 %) exposures. The most common classes of agents were sedative-hypnotics (1,422 entries in 13 % of cases) non-opioid analgesics (1,295 entries in 12 % of cases), opioids (1,086 entries in 10 % of cases) and antidepressants (1,039 entries in 10 % of cases). N-acetylcysteine (NAC) was the most common antidote administered in 2012, as it was in previous years, followed by the opioid antagonist naloxone, sodium bicarbonate, physostigmine and flumazenil. Anti-crotalid Fab fragments were administered in 109 cases or 82 % of cases in which a snake envenomation occurred. There were 57 deaths reported in the Registry in 2012. The most common associated agent alone or in combination was the non-opioid analgesic acetaminophen, being reported in 10 different cases. Other common agents and agent classes involved in death cases included ethanol, opioids, the anti-diabetic agent metformin, sedatives-hypnotics and cardiovascular agents, in particular amlodipine. There were significant trends identified during 2012. Abuse of over-the-counter medications such as dextromethorphan remains prevalent. Cases involving dextromethorphan continued to be reported at frequencies higher than other commonly abused drugs including many stimulants, phencyclidine, synthetic cannabinoids and designer amphetamines such as bath salts. And, while cases involving synthetic cannabinoids and psychoactive bath salts remained relatively constant from 2011 to 2012 several designer amphetamines and novel psychoactive substances were first reported in the Registry in 2012 including the NBOME compounds or "N-bomb" agents. LSD cases also spiked dramatically in 2012 with an 18-fold increase from 2011 although many of these cases are thought to be ultra-potent designer amphetamines misrepresented as "synthetic" LSD. The 2012 Registry included over 400 Adverse Drug Reactions (ADRs) involving 4 % of all Registry cases with 106 agents causing at least 2 ADRs. Additional data including supportive cares, decontamination, and chelating agent use are also included in the 2012 annual report. The Registry remains a valuable toxico-surveillance and research tool. The ToxIC Registry is a unique tool for identifying and characterizing confirmed cases of significant or potential toxicity or complexity to require bedside care by a medical toxicologist.
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Amlodipine (once daily) and captopril (twice daily) had comparable efficacy and safety in reducing the blood pressure of patients with mild and moderate essential hypertension. Amlodipine administered once daily is an effective and well-tolerated treatment.
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Calcium channel blockers (CCBs) inhibit voltage-dependent L-type calcium channels. This leads to vascular smooth muscle relaxation and negative inotropic and chronotropic effects in the heart. The latter are counteracted in vivo by a vasodilatation-triggered, baroreceptor-mediated reflex increase in sympathetic tone, resulting in indirect cardiostimulation. The mean vascular/cardiac effect ratios of the first-generation CCBs-verapamil, nifedipine, and diltiazem-are relatively low and amount to approximately 3, 10, and 3, respectively. The pharmacokinetic properties of verapamil, nifedipine, and diltiazem are similar. The drugs are almost completely absorbed after oral administration, but their bioavailability is reduced because of first-pass hepatic metabolism. The onset of action of verapamil, nifedipine, and diltiazem, at least in immediate-release formulations, is relatively fast (0.5-2 hours), and their elimination half-lives range from 2 to 7 hours. The second-generation CCBs (e.g., amlodipine, felodipine, and nisoldipine) have a slower onset of action (due to either intrinsic properties of the drug or a slow-release formulation), a longer duration of action, and greater vascular/cardiac effect ratios. These features may provide therapeutic benefits, for example, a less pronounced increase in sympathetic tone and reflex tachycardia, and reduced likelihood of negative inotropic effects. These agents can therefore probably be used in patients with left ventricular dysfunction.
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Both enalapril and amlodipine preserve LV volumes and function during healing after reperfused MI, but enalapril more effectively limits hypertrophy, attenuates infarct wall thickness and preserves shape.
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Dasatinib is a novel second-generation inhibitor of multiple tyrosine kinases, indicated for the treatment for Philadelphia chromosome-positive (Ph+) chronic myeloid leukaemia (CML), acute lymphoblastic leukaemia (ALL) and lymphoid blast CML with resistance or intolerance to prior therapy. Although dasatinib is a potent, efficacious and generally well-tolerated drug, patients are also subject to various adverse effects. The most common pulmonary-related side effect is pleural effusion (PE). Renal failure has been reported rarely as a side effect of dasatinib treatment. We report the first case of a patient with imatinib-resistant CML who developed PE and acute renal failure (ARF) simultaneously, after being placed on dasatinib therapy.
In this randomized, double-blind, parallel group study, hypertensive patients were randomly assigned to receive manidipine 20 mg (n = 54) or amlodipine 10 mg (n = 50) for 4 weeks. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were determined by constant-infusion input-clearance technique with p-aminohippurate (PAH) and inulin. P(glom) and resistances of the afferent (R(A)) and efferent (R(E)) arterioles were calculated according to the model established by Gomez.
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The reduction of SiDBP after 8 weeks of treatment with S(-)-amlodipine nicotinate was noninferior compared with that of racemic amlodipine besylate in these adult Korean patients with mild to moderate hypertension. The SiDBP response rate and the reduction of SiSBP after 8 weeks of treatment with S(-)-amlodipine nicotinate were not significantly different from those with racemic amlodipine besylate. Both treatments were generally well tolerated.
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Proteinuria data were not available, and combination therapies were not tested.
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The aim of this study was to examine the effects of amlodipine (AML) in rat testicular torsion/detorsion damage. In this study, rats were divided into eight groups: (i) sham; (ii) testicular ischaemia, 2 h of ischaemia; (iii) testicular ischaemia/reperfusion (I/R), 2 h of ischaemia followed by 2 h of reperfusion; (iv) ischaemia + AML (5 mg kg(-1)) administered 30 min before ischaemia; (v) ischaemia + AML (10 mg kg(-1)) administered 30 min before ischaemia; (vi) and (vii) I/R + AML (5 mg kg(-1)) and I/R + AML (10 mg kg(-1)) administered 1.5 h after the induction of ischaemia, respectively, and at the end of a 2-h ischaemia period and a 2-h reperfusion period applied; and (viii) sham + AML (10 mg kg(-1)). Significant decreases in levels of superoxide dismutase and glutathione were observed in ischaemia and reperfusion groups when compared with healthy controls. These antioxidant levels increased in AML groups while malondialdehyde levels significantly decreased. While increases in tumour necrosis factor-alpha and transforming growth factor-beta levels were found in the torsion and detorsion groups, significant decreases in the levels of these inflammatory cytokines were observed in the treatment groups. These results demonstrate that AML significantly produced protective effects on testis tissue damage that occurs in the torsion/detorsion model via biochemical, histopathological and molecular pathways.
Forty diabetic hypertensive subjects were assigned to two groups. Group A: rosiglitazone (RSG) 4 mg + Telm 80 mg; Group B: RSG 4 mg + Aml 10 mg. All the patients were already treated with metformin, but not with antihypertensive drugs.
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Although awareness of hypertension in Black patients has increased, blood pressure (BP) is frequently inadequately controlled.
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Biomarkers are being increasingly used in the study of cardiovascular disease because they provide readily quantifiable surrogate endpoints and allow accurate assessment of the effects of therapy on particular pathological processes. However, in order to be useful, biomarkers must be relevant, predictable, accurate, and reproducible. There is compelling evidence from large-scale clinical trials that inhibitors of the renin-angiotensin system [angiotensin-converting enzyme inhibitors and angiotensin type II receptor blockers (ARBs)] and calcium channel blockers (CCBs) may have beneficial effects beyond blood pressure control in the treatment of hypertension. Biomarkers are expected to provide further insight into these beneficial effects and allow for quantitative assessment. This review summarizes the published clinical evidence on the effects of various antihypertensive drugs, particularly ARBs (e.g. losartan and olmesartan medoxomil) and CCBs (e.g. amlodipine), alone and in combination with other agents (e.g. hydrochlorothiazide), on central aortic pressure and the biomarkers high-sensitivity C-reactive protein (hsCRP), adiponectin, cystatin C, homeostasis model assessment of insulin resistance (HOMA-IR), procollagen, tumor necrosis factor-α, and interleukin-6. Of these biomarkers, the benefits of antihypertensive therapy on hsCRP, adiponectin, and HOMA-IR reflect a potential for quantifiable long-term vascular benefits.
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We conducted a randomised, double blind, placebo controlled trial to assess the efficacy and safety of cilostazol, a selective inhibitor of phosphodiesterase 3, in patients with vasospastic angina (VSA).
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The Cmax and AUClast and of simvastatin acid in the non-concurrent amlodipine dosing group were 63.2% and 66.0%, respectively, of the values obtained in the concurrent group (1.2 +/- 1.0 vs. 1.9 +/- 0.9 ng/ml and 10.3 +/- 8.3 vs. 15.6 +/- 7.5 h ng/ml, respectively, mean +/- standard deviation). Changes from baseline in lipid profile and blood pressure were comparable between the groups.
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To investigate plasma brain natriuretic peptide (BNP) concentrations in association with blood pressure (BP) at baseline and after antihypertensive drug treatment.