![]() ![]() When used in combination, enalapril was shown to attenuate the extent of drug-induced hypokalemia caused by hydrochlorothiazide and the antihypertensive effects of both drugs were potentiated. It also augmented the glomerular filtration rate in patients with a glomerular filtration rate less than 80 mL/min. In the kidneys, enalapril was shown to increase renal blood flow and decrease renal vascular resistance. Vasotec IV is not reported to produce hypokalaemia, hyperglycaemia, hyperuricaemia or hypercholesterolaemia. Vasotec IV is not highly associated with the risk of bradycardia unlike most diuretics and beta-blockers and it does not produce rebound hypertension upon discontinuation of therapy. In clinical studies, enalapril reduced left ventricular mass, and did not affect cardiac function or myocardial perfusion during exercise. Furthermore, enalapril was shown to increase cardiac output and stroke volume while decreasing pulmonary capillary wedge pressure in patients with congestive heart failure refractory to conventional treatment with digitalis and diuretics. In patients with severe congestive heart failure and inadequate clinical response to conventional antihypertensive therapies, treatment with enalapril resulted in improvements in cardiac performance as observed by a reduction in both preload and afterload, and improved clinical status long-term. The duration of hypertensive effect in the systolic and diastolic blood pressure persists for at least 24 hours following initial administration of a single oral dose, and repeated daily administration of enalapril confers an additional reduction in blood pressure and a steady-state antihypertensive response may take several weeks. Individuals with low-renin hypertensive population were still responsive to enalapril. Vasotec IV lowers blood pressure in all grades of essential and renovascular hypertension, and peripheral vascular resistance without causing an increase in heart rate. Vasotec IV is an antihypertensive agent that exhibits natriuretic and uricosuric properties. ![]() The beneficial effects of enalapril in hypertension and heart failure appear to result primarily from suppression of the renin-angiotensin aldosterone system ![]() Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. ACE is a peptidyl dipeptidase that catalyses the conversion of angiotensin I to the vasoconstrictor substance angiotensin II. Vasotec IV, after hydrolysis to enalaprilate, inhibits Angiotensin Converting Enzyme (ACE). ![]()
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