Enalapril Research Articles

Effects of Infusing a-Atrial Natriuretic Peptide in Primary Hypertension During Converting Enzyme Inhibition

The effect of atrial natriuretic peptide (ANP), before and after converting enzyme (CE) inhibition, was investigated in six primary hypertensive patients taking a constant diet. In this placebo-controlled, single-blind, randomized study, the patients received, on three different days, i.v. infusions of (a) placebo, or (b) alpha-human ANP, 150 micrograms over 30 min, or (c) alpha-human ANP after acute CE inhibition by enalapril (EN) 20 mg P.O., 4 h before ANP infusion. ANP infusion increased urinary sodium (p less than 0.001) and volume excretion. Blood pressure (BP), heart rate, stroke volume and shortening fraction (echocardiography), plasma renin activity (PRA), and plasma aldosterone did not change significantly. Urinary norepinephrine and dopamine were significantly increased (p less than 0.05) after ANP infusion. BP was significantly reduced after EN in every patient (p less than 0.05). ANP infusion during CE inhibition induced a more sustained increase of sodium excretion and diuresis with respect to ANP infusion alone (p less than 0.05). PRA was significantly reduced while no further reduction of BP was observed. These data suggest that CE inhibition may increase the natriuretic and diuretic effect of ANP in hypertensive patients.

ENALAPRIL AND STEPPED-CARE HYPERTENSION THERAPY.

With more drugs on the market, the approach to antihypertensive therapy has become both more confusing and more effective. In a randomized, double-blind trial of 205 patients, enalapril was compared with hydrochlorothiazide …

The metabolic effects of enalapril.

The metabolic effects of Enalapril (EN) were compared in a cross over study with those of Propranolol (PPL). Long term treatment with the ACEI did not modify the lipid and glucose profile and increased urate excretion, while PPL increased triglycerides and decreased urate clearance.

Efficacy of Isosorbide-5-Mononitrate (Is5Mn) in Patients Treated with Diuretics and Enalapril

Efficacy of Isosorbide-5-Mononitrate (Is5Mn) in Patients Treated with Diuretics and Enalapril

Captopril and Enalapril Appear Equally Effective in Hypertension

Captopril and Enalapril Appear Equally Effective in Hypertension

Focus on Enalapril - Active in Hypertension and CHF

Focus on Enalapril - Active in Hypertension and CHF

Examining the Behaviour of Enalapril

Examining the Behaviour of Enalapril

Enalapril see also Captopril

Enalapril see also Captopril

Enalapril: compares well with hydrochlorothiazide in hypertension

Enalapril: compares well with hydrochlorothiazide in hypertension

Enalapril: more studies of its action

Enalapril: more studies of its action

The effect of enalapril on serum prolactin.

Twelve healthy male volunteers received single daily oral doses of enalapril (EN) 10 mg for 8 consecutive days. Serum samples for prolactin (PRL) assay were taken on day 0 (baseline) at 12.00 h and 16.00 h, and on days 1 and 8 at 08.00 h (pre-drug), 12.00 h and 16.00 h. The 08.00 h values on day 1 served as the pre-drug baseline. There were no significant changes from baseline in serum PRL levels on days 1 and 8. All mean serum PRL levels on day 8 were significantly (P less than 0.01) lower than the upper limit of the normal range (2-15 ng/ml) found for healthy males in this laboratory. It is concluded that therapeutic doses of EN (10 mg/day, p.o.) for 8 consecutive days do not raise mean serum PRL levels above the normal range in healthy male volunteers.

Urinary excretion of prostacyclin and thromboxane A 2 metabolites after angiotensin converting enzyme inhibition in hypertensive patients

The contribution, if any, of various prostaglandins to the antihypertensive effects of angiotensin converting enzyme inhibitors (ACEI) is controversial. We studied the effect of the ACEI captopril (CAP) on the urinary excretion of 6-keto-PGF 2α (6-KF), the major metabolite of the vasodilatory prostaglandin, prostacyclin, and thromboxane B 2 (TxB 2), the stable metabolite of the vasoconstrictor TxA 2, in 8 patients with essential hypertension after placebo, two weeks of CAP 25 mg t.i.d. alone, and the same dose of CAP in combination with hydrochlorothiazide (HCTZ) 50 mg/day. Mean 6-KF and TxB 2 (nmol/8 hr post-dosing, respectively) did not differ significantly with any treatment; the mean ratio of 6-KF/TXB 2 was also unchanged. Likewise, the excretion of these prostaglandins was also evaluated after placebo, the ACEI enalapril (ENA) (5 or 10 mg/day), and the combination of ENA and HCTZ in another group of 8 patients with essential hypertension. Mean 6-KF and TxB 2 (nmol/24 hr post-dosing, respectively) showed no significant treatment-related differences; the mean ratio was again unchanged. No correlation existed between the magnitude of blood pressure responses with any treatment and either 6-KF or TxB 2 excretion. Thus, the antihypertensive action of ACEI, alone or in combination with HCTZ, does not appear to involve alterations in these vasoactive prostaglandins.