Effect of Chronic Treatment with Captopril on Reactivity of Aortic Smooth Muscle from Normotensive and Renal Hypertensive Rats

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Abstract
Acute administration of the angiotensin I converting enzyme inhibitor, captopril (2 x 10-4 M), was shown in an earlier study to attenuate the contractile responses of aortic rings of rats to α -adrenergic agonists in vitro. The objective of the present study was to determine the effect of chronic treatment with captopril on reactivity of aortic rings from both normotensive and renal hypertensive rats when captopril was no longer present. Four groups of rats were used (1) normotensive, untreated (2) normotensive, captopril-treated (48 mg/kg b.w. per day for five weeks) (3) hypertensive (bilateral renal encapsulation for five weeks), untreated and (4) hypertensive, captopril-treated Renal encapsulation was associated with a significant increase in systolic blood pressure, which was prevented by concomitant treatment with captopril. At the end of the five weeks treatment aortic rings, 4 mm in length, were washed for 2 h to remove the captopril, following which contractile responses to various vasoactive agents were studied in vitro. Chronic treatment with captopril attenuated significantly contractile responses to both norepinephrine (10-9 to 10-5 M) and phenylephrine (10-8 to 10-4 M) but had no effect on isoproterenol-induced relaxation of KCI-depolarized tissue in the presence of 10-5 M phentolamine. Contractile responses to angiotension I (10-10to 10-7 M) did not differ statistically among the four groups. Following addition of captopril (2 x 10-4 M) to the bath for 30 min, contractile responses to angiotensin I were attenuated in all four groups of rings. This study indicates that chronic treatment with captopril, like acute administration in vitro, attenuates specifically α -adrenergic responsiveness of rat aortic rings in vitro. As this attenuation persists in the absence of captopril (when converting enzyme is no longer inhibited), it does not appear to be directly dependent on alterations in conversion of angiotensin I to angiotensin II

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