Effect of in vitro administration of captopril on vascular reactivity of rat aorta

Abstract

The effect of acute administration of captopril, an angiotensln converting enzyme inhibitor, on vascular responses of rings of rat aortic smooth muscle was tested in vitro. Dose-response curres for various rasoactive agents were obtained before and after exposure to captopril (2 X 10-4M) for 30 minutes. In the presence of captopril, contractile responses to angiotensln I (5 X 10-10to 5 X 10-4M) were attenuated significantly, probably as a result of decreased local conversion of angiotensin I to angiotensin H. Contractile responses to angiotensin II (10-2to 5 X 10-4M) were not affected by captopril. All responses to norepinephrine (10-4to 10-4M) and phenyiephrine (10-4to 10-4M) were attenuated significantly from control in the presence of captopril. In the presence of the α-adrenergic antagonist, phentolamine, captopril did not affect either the contractile responses to KG (30 to 100 mM) or the isoproterenol-induced (10-2to 10-3M) relaxation of KG-depolarized tissue. These results suggest that captopril decreased vascular responsiveness to a-adrenergic agonists but not to β-adrenergic agonists. Low concentrations of bradykinln (10-20to 10-8M) Induced contraction in KCl-depolarized tissue while higher concentrations (10-7and 10-4M) induced relaxation. In the presence of captopril, relaxation occurred at all concentrations of bradykinln (10-10to 10-4M), probably as a result of decreased degradation of the bradykinln. These data suggest depression of α-adrenergic responsiveness in vascular smooth muscle as another potential antihypertensive action of captopril. © 1982 American Heart Association, Inc.