Affiliation:
1. Department of Pharmacology-Physiology, University of Pittsburgh 15261.
Abstract
The effects of angiotensin II on pressor responses to electrical field stimulation (1-32 Hz) of the adrenal gland were assessed in pithed male Sprague-Dawley rats. Stimulation elicited frequency-related pressor responses and increments in plasma catecholamines. Interruption of the renin-angiotensin system with the converting enzyme inhibitor captopril or the receptor antagonist saralasin significantly attenuated the pressor responses to adrenal stimulation and injected epinephrine to an equivalent extent. This observation, along with the finding that captopril did not alter the plasma catecholamine increments produced by adrenal stimulation, suggested that endogenously generated angiotensin II was not affecting adrenal catecholamine release. Instead angiotensin II appears to interact at the level of the vascular smooth muscle, because reinfusion of angiotensin II (20 ng.kg-1.min-1 iv) in captopril-treated animals restored responsiveness to stimulation and epinephrine. Infusion of vasopressin also restored pressor activity after captopril; therefore the interaction does not appear to be specific for angiotensin II but may depend on the background tone of the vascular smooth muscle. Moreover, decreasing blood pressure with sodium nitroprusside reversibly attenuated the pressor responses to both adrenal stimulation and epinephrine. The results suggest that endogenously formed angiotensin II facilitates the vasoconstrictor activity of epinephrine by increasing vascular tone.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Cited by
11 articles.
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