AJP - Regulatory, Integrative and Comparative Physiology, Vol 246, Issue 1 13-R19, Copyright © 1984 by American Physiological Society
Central actions of angiotensin II oppose baroreceptor-induced sympathoinhibition
R. D. Stein, R. B. Stephenson and L. C. Weaver
Angiotensin II causes increased arterial pressure which may be mediated, in
part, by effects on central sympathetic neurons or by interference with
central or peripheral components of the baroreceptor reflex. This
investigation was undertaken to determine actions of angiotensin II on
sympathetic splanchnic efferent and carotid sinus afferent activity in
chloralose-anesthetized cats. Neural responses during increases in arterial
pressure caused by intracarotid or intravenous administration of
angiotensin II were compared with responses to equivalent increases in
arterial pressure induced by intravenously injected dextran or
phenylephrine. Intracarotid injections of angiotensin II caused variable
splanchnic sympathetic responses consisting of increased, decreased, or
unchanged activity. In contrast, intravenous infusions of dextran or
phenylephrine consistently inhibited sympathetic activity. Carotid sinus
afferent activity was increased similarly by intracarotid angiotensin II
and intravenous dextran or phenylephrine. Sympathetic and baroreceptor
afferent responses to intravenously injected angiotensin II were not
significantly different from responses to dextran or phenylephrine. These
data demonstrate that angiotensin II can act centrally to excite
sympathetic outflow or to interfere with inhibitory influences of arterial
baroreceptors.
