Double-blind crossover study of the interaction between perindopril and amlodipine on blood pressure and hormones related to fluid and electrolyte balance in patients with essential hypertension

Abstract

This study was to investigate the interaction between opposite result was obtained for clinic BP at trough, whereby the addition of amlodipine to perindopril low doses of perindopril (2 mg daily) and amlodipine (2.5 mg daily) on ambulatory blood pressure (BP), clinic reduced erect systolic BP (P = 0.036) and both supine and erect diastolic BP (P = 0.038) whereas the addition BP, serum angiotensin-converting enzyme (ACE), plasma levels of renin (PRA), angiotensin II (Ang II), of perindopril to amlodipine was without effect. The addition of perindopril to amlodipine decreased aldosterone, and atrial natriuretic peptide (␣-h ANP) in subjects with essential hypertension. The study design serum ACE by 72% and increased PRA two-fold, without change in plasma levels of Ang II, aldosterone or ␣-h was a parallel, two-period, placebo-controlled, doubleblind crossover design, with 11 subjects receiving per-ANP. The addition of amlodipine to perindopril increased plasma aldosterone 1.7-fold but did not affect indopril and 10 receiving amlodipine during the run-in phase.serum ACE, PRA, Ang II, or ␣-h ANP. These interactions between perindopril and amlodipThe addition of amlodipine to perindopril had no effect on ambulatory BP, whereas the addition of perinine may have been conditioned by the specific effects of the therapy first given, as well as by the different cirdopril to amlodipine reduced both systolic (P = 0.027) and diastolic (P = 0.049) ambulatory BP. By contrast, the cumstances of BP measurement (ambulatory vs clinic).

The effect of amlodipine and the combination of amlodipine and enalapril on the renin‐angiotensin‐aldosterone system in the dog

“…Previous studies are few and have provided controversial results with regard to calcium antagonists' effect on the RAAS. Results have varied with some studies demonstrating activation of the RAAS (Cappuccio et al, 1991;Kokot et al, 1997) while others have been unable to demonstrate activation (Donati et al, 1992;Letizia et al, 1993;Damasceno et al, 1999) or have produced inconsistent results (Stokes et al, 1998). Furthermore we postulated that addition of an ACE inhibitor would blunt the effects of amlodipine on the RAAS.…”

Molecular and clinical investigations in patients with low-renin hypertension

“…Both acute and chronic (four weeks) administration of nifedipine to patients with primary hyperaldosteronism (due to adrenal adenoma or hyperplasia) reduced plasma aldosterone levels in one study [13], and chronic (two months) treatment with amlodipine gave a similar result [14]. However, conversely, some data in normotensive controls and in patients with essential hypertension suggest that administration of calcium channel blockers may actually increase aldosterone levels [15,16]. This raises the question of whether patients with aldosterone-producing adrenal adenomas respond differently to calcium channel blockade compared to normal subjects and subjects with other types of hypertension.…”