Central actions of angiotensin II oppose baroreceptor-induced sympathoinhibition

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.