AJP - Regulatory, Integrative and Comparative Physiology, Vol 254, Issue 1 95-101, Copyright © 1988 by American Physiological Society
Angiotensin II facilitation of pressor responses to adrenal field stimulation in pithed rats
R. R. Vollmer, S. P. Corey and S. J. Fluharty
Department of Pharmacology-Physiology, University of Pittsburgh 15261.
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.
