Cardiac and haemodynamic effects of enalapril.
The haemodynamic effects of enalapril were evaluated by sequential radionuclide studies in 10 patients followed for three to seven months. The pattern of response was remarkably similar to that of angiotensin antagonists and other oral converting enzyme inhibitors; it consisted of a reduction in peripheral resistance, minimal blood volume changes and no significant increase in either cardiac output or heart rate. The haemodynamic and neurohumoral responses to upright tilt remained normal, despite the lack of supine tachycardia in response to peripheral vasodilation. The pattern of response suggests that the haemodynamic effects of enalapril resulted from interference with angiotensin II (AII) generation rather than from a direct drug effect. Serial echocardiographic studies showed a significant regression in left ventricular (LV) hypertrophy in six out of seven hypertensive patients followed sequentially for three to seven months. Ventricular performance was well preserved despite the reduction in ventricular mass, as indicated by maintenance of the normal relationship of LV fractional shortening (% Sh) to LV end-systolic stress.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001810:Blood Volume / Q000187:drug effects; D006332:Cardiomegaly / Q000188:drug therapy; D004452:Echocardiography; D004656:Enalapril / Q000494:pharmacology* / Q000627:therapeutic use; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D006978:Hypertension, Renovascular / Q000188:drug therapy; D051381:Rats
D004656:Enalapril