We examined the effects of an orally active inhibitor of converting enzyme, captopril (D-3-mercapto-2-methylpropanoyl-L-proline), in pentobarbital-anesthetized rats. Intravenous (i.v.) administration of captopril (0.1, 0.3, 1.0, 3.0 mg/kg) resulted in a dose-dependent inhibition of the pressor responses to angiotensin I (1.0 μg/kg, i.v.); at 1.0 mg/kg, captopril markedly potentiated the magnitude and duration of vasodepressor responses elicited by bradykinin (0.3 μg/kg, i.v.). Captopril effected a marked elevation of plasma renin activity by its blocking action on the angiotensin II-mediated negative feedback of renin release without markedly altering systemic blood pressure and heart rate. Propranolol (1.5 mg/kg, i.v.), at a dose which almost completely inhibited isoproterenol (0.15 μg/kg/min, i.a.)-induced renin release, tended to suppress the captopril-induced renin release. However, indomethacin (5.0 mg/kg, i.v.) failed to change the captopril-induced renin release. These findings suggest that captopril specifically inhibits converting enzyme and kininase II, and that captopril-induced renin release is partially associated with the beta-adrenergic system without mediation by prostaglandins.
|Number of pages||16|
|Journal||Archives Internationales de Pharmacodynamie et de Therapie|
|Publication status||Published - 1981 Dec 1|
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