Beneficial Effects Of Amlodipine Research Articles

Use of amlodipine + ramipril single-pill combination for prevention of stroke in hypertension patient (clinical case)

Arterial hypertension is one of the most significant modifiable risk factors for stroke. The article provides a clinical example of using a fixed combination of amlodipine + ramipril in real clinical practice in a patient suffering from arterial hypertension, occurring with dyslipidemia, hyperuricoemia, microalbuminuria. High antihypertensive activity of a fixed combination of amlodipine + ramipril was shown. A literature review of the beneficial effect of amlodipine and lisinopril on the risk of stroke, as well as the beneficial effect of this combination of drugs on the course of chronic kidney disease developing in patients with arterial hypertension, is presented.

The role of amlodipine (norvasc) in Cardiology

The review concerns amlodipine - the representative of the third generation of dihydropyridines. Amlodipine, being considered a hypotensive drug, has a broad spectrum of clinical effects beyond the hypotensive effects. It is shown that the drug has different pleiotropic effects, allowing using it as an anti-atherosclerotic and organoprotective funds. The data on the beneficial effect of amlodipine in pathology, is not included in the group of cardiovascular diseases - Raynaud's syndrome, migraine headaches, tendency to vomit.

An Additional LDL-Lowering Effect of Amlodipine; Not Only an Antihypertensive?

Hypertension is a modifiable risk factor for cardiovascular diseases and is associated with several metabolic disorders like dyslipidemia. Higher levels of triglyceride and low-density lipoprotein (LDL) are quite strong factors for the development of cardiovascular diseases. In this study, we investigated the effects of valsartan and amlodipine on the lipid profile in patients with newly diagnosed essential hypertension. We observed a beneficial effect of amlodipine on the lipid profile with a significant reduction of LDL compared to valsartan. In the treatment of hypertension, prior knowledge of the plasma cholesterol levels can be important in antihypertensive drug choice.

Possible beneficial effects of amlodipine, lisinopril, and their Combination on lipid profile in hypertensive patients

It is well known that monotherapy does not provide therapeutic response in all hypertensive. Somepatients show an excellent response, while in others there is a poor response. Combinationantihypertensive therapy is administered when blood pressure is inadequately controlled bymonotherapy to achieve a balanced and additive antihypertensive effect with minimum adverse effects.Both angiotensin converting enzyme (ACE) inhibitors and dihydropyridine type of calcium antagonistsare well established and widely used in monotherapy. An understanding of differences in themechanism of action of these agents allows a logical approach for the use of these agents as acombination therapy. This study was designed to evaluate the possible beneficial effects of long actingcalcium channel blocker, amlodipine and the long acting Angiotensin converting enzyme (ACE)inhibitor, lisinopril given either alone or in combination in patients with essential hypertension on lipidprofile (LDL-C and HDL-C) and on other parameters using a randomized double blind, crossoverstudy. The study includes 150 patients with systolic blood pressure (SBP)>140 mmHg and diastolicblood pressure (DBP) >90 mmHg received amlodipine 5 mg, lisinopril 5 mg and their combinationprior randomization schedule. Systolic, diastolic blood pressure and pulse rate were recorded at weeklyintervals while, serum levels of urea, creatinine, LDL-C and HDL-C where recorded at monthlyintervals, the duration of this study was 3 months. Results were obtained using paired students t-test,differences were considered significant with (p<0.05).A significant decline in SBP and DBP in all treatment groups (p<0.05) was recorded, the reductiontend to be more pronounced in the combination group. Moreover, there was a significant effect ofcombination on the heart rate, serum level of urea and creatinine, beside that, the level of HDL wassignificantly elevated with amlodipine and combination. We concluded that combination had additionalblood pressure lowering effect when compared either with amlodipine or lisinopril alone, in addition tothe greater effect on lipid profile which demonstrated that this combination is potentialantiatherosclerotic agent.

Effects of amlodipine on tubulointerstitial lesions in normotensive hyperoxaluric rats.

Although controversial, a number of reports have suggested that calcium antagonists can retard or prevent the progression of various renal diseases in experimental models. Nevertheless, there are few data related to tubulointerstitial changes in these studies. On the other hand, hyperoxaluria is a recognized cause of tubulointerstitial lesions, and this could contribute to the development of hypertension and chronic renal failure. The aim of the present study was to evaluate a possible beneficial effect of amlodipine, a 1,4-dihydropyridine class of calcium antagonist, in a model of primary tubulointerstitial lesion produced by hyperoxaluria. Two-month-old male Sprague-Dawley rats were separated into 4 groups for a 4-week period: G1 (control; tap water only); G2 (hyperoxaluric); G3 (hyperoxaluric plus amlodipine treatment); and G4 (amlodipine treatment). G2 and G3 rats were given 1% ethylene glycol (a precursor for oxalates) in drinking water, and G3 and G4 rats were given amlodipine 2 mg. kg(-1). d(-1) by gavage. At the end of the study, we evaluated by semiquantitative scores (0 to 4) the different renal tubulointerstitial lesions, urinary albumin excretion, renal function by creatinine clearance, and blood pressure. Rats belonging to the hyperoxaluric group treated with amlodipine (G3) had fewer tubulointerstitial lesions, as follows: (1) inflammatory infiltrate score: 3.31+/-0.07 versus 0.23+/-0.12; P<0.05; (2) tubular atrophy score: 3.33+/-0.33 versus 0.50+/-0.22, P<0.05; (3) interstitial fibrosis score: 2.76+/-0.34 versus 0.31+/-0. 16, P<0.05; (4) oxalate deposits score: 3.66+/-0.33 versus 0.09+/-0. 08, P<0.05; (5) lower urinary albumin excretion (11.3+/-2 versus 27+/-4.5 mg/d, P<0.01); and (6) higher creatinine clearance (1. 22+/-0.08 versus 1.13+/-0.08, P<0.01) compared with the hyperoxaluric group untreated with amlodipine (G2). On the other hand, there were no significant changes in blood pressure in any group. In view of these data, we suggest that amlodipine, probably by nonhemodynamic mechanisms of action, can provide an important benefit in the prevention of epithelial tubular cell injury and inflammatory response and therefore in the prevention of the progressive tubulointerstitial fibrosis caused by oxalates.

Beneficial effects of amlodipine on cardiac remodeling in dilated cardiomyopathy

Beneficial effects of amlodipine on cardiac remodeling in dilated cardiomyopathy

Role of Cytokines in the Mechanism of Action of Amlodipine: The PRAISE Heart Failure Trial

Objectives. We sought to determine whether the beneficial effects of amlodipine in heart failure may be mediated by a reduction in tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) levels. We postulated that TNF-alpha and IL-6 levels may also have predictive value in patients with congestive heart failure (CHF).Background. The molecular mechanism for progression of CHF may involve cytokine overexpression. The effect of amlodipine on cytokine levels in patients with CHF is unknown.Methods. In the Prospective Randomized Amlodipine Survival Evaluation (PRAISE) trial, we used enzyme-linked immunosorbent assay to measure plasma levels of TNF-alpha in 92 patients and IL-6 in 62 patients in New York Heart Association functional classes III and IV randomized to receive amlodipine (10 mg/day) or placebo. Blood samples were obtained for cytokine measurement at baseline and at 8 and 26 weeks after enrollment.Results. The baseline amlodipine and placebo groups did not differ in demographics and cytokine levels. Mean (±SD) plasma levels of TNF-alpha were 5.69 ± 0.32 pg/ml, and those of IL-6 were 9.23 ± 1.26 pg/ml at baseline. These levels were elevated 6 and 10 times, respectively, compared with those of normal subjects (p < 0.001). Levels of TNF-alpha did not change significantly over the 26-week period (p = 0.69). However, IL-6 levels were significantly lower at 26 weeks in patients treated with amlodipine versus placebo (p = 0.007 by the Wilcoxon signed-rank test). An adverse event—CHF or death—occurred more commonly in patients with higher IL-6 levels.Conclusions. Amlodipine lowers plasma IL-6 levels in patients with CHF. The beneficial effect of amlodipine in CHF may be due to a reduction of cytokines such as IL-6.(J Am Coll Cardiol 1997;30:35–41)

Beneficial effects of amlodipine in a murine model of congestive heart failure induced by viral myocarditis. A possible mechanism through inhibition of nitric oxide production.

Although calcium channel blockers have not been shown to be beneficial for the treatment of patients with heart failure, a recent clinical trial demonstrated a favorable effect of amlodipine on the survival of patients with heart failure resulting from nonischemic dilated cardiomyopathy. We investigated the effects of amlodipine on a murine model of congestive heart failure induced by the M variant of encephalomyocarditis virus (EMCV). Four-week-old male DBA/2 mice were inoculated with EMCV and administered amlodipine, diltiazem, or vehicle PO for 2 weeks. The heart weight-to-body weight ratio and the histopathological grades of myocardial lesions were significantly lower and survival was significantly increased in the amlodipine-treated group (P < .01, P < .05, and P < .05, respectively) than in the control group. In vitro, amlodipine added to murine J774A.1 macrophages concomitant with EMCV inhibited nitrite formation in a concentration-dependent manner, but diltiazem did not. Furthermore, NG-monomethyl-L-arginine, an inhibitor of NO synthesis, decreased myocardial lesions significantly in this murine model. Immunohistochemistry revealed that the number of cells stained with antibody against an inducible NO synthase decreased significantly in the amlodipine-treated group compared with that in the control group (P < .01). Amlodipine appears to have a protective effect against myocardial injury in this animal model of congestive heart failure. The therapeutic effect of amlodipine may be in part resulting from inhibition of overproduction of NO.