Baroreceptor denervation profoundly enhances cardiovascular responses to central angiotensin II.

The purpose of this study was to examine the influence of arterial baroreflexes on the pressor and regional hemodynamic responses to centrally administered angiotensin II (ANG II) in the conscious rat. Fourteen days after sinoaortic baroreceptor denervation (SAD) or the equivalent sham surgery, the pressor and hindquarters vascular resistance responses to intravenous administration of ANG II were augmented in the SAD group. The pressor and vasoconstrictor responses to intracerebroventricular ANG II were also augmented after SAD; however, the SAD animals were more than 1,000-fold more sensitive than the sham group to the pressor effects of intracerebroventricular ANG II. Further experiments demonstrated that 1) the enhanced pressor response to intracerebroventricular ANG II in the baroreceptor-denervated group was due to similar increases in sympathetic outflow and vasopressin mediated vasoconstriction, 2) the increased sensitivity to central ANG II occurs as soon as 1 h after SAD, and 3) the enhanced pressor effects to intracerebroventricular ANG II also occur with intracerebroventricular hypertonic saline. We conclude that arterial baroreflexes exert a potent central inhibitory effect on the central pressor actions of ANG II that are greater than can be accounted for by the peripheral reflex arc. Finally, because of the rapid onset of the increased responsiveness to central ANG II after SAD, we propose that baroreflex buffering of central pressor stimuli may be tonically involved in circulatory control.