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Submitted on January 18, 2005
From the Circulatory Control Laboratory, Department of Physiology, University of Auckland, New Zealand. * To whom correspondence should be addressed. E-mail: c.barrett{at}auckland.ac.nz.
Abstract--Arterial baroreflexes are well established to provide the basis for short-term control of arterial pressure; however, their role in long-term pressure control is more controversial. We proposed that if the sustained decrease in renal sympathetic nerve activity (RSNA) we observed previously in response to angiotensin II-induced hypertension is baroreflex mediated, then the decrease in RSNA in response to angiotensin II would not occur in sinoaortic-denervated (SAD) animals. Arterial pressure and RSNA were recorded continuously via telemetry in sham and SAD rabbits living in their home cages before, during, and after a 7-day infusion of angiotensin II (50 ng · kg-1 · min-1). The arterial pressure responses in the 2 groups of rabbits were not significantly different (82±3 mm Hg sham versus 83±3 mm Hg SAD before angiotensin II infusion, and 101±6 mm Hg sham versus 100±4 mm Hg SAD day 6 of angiotensin II). In sham rabbits, there was a significant sustained decrease in RSNA (53±7% of baseline on day 2 and 65±7% on day 6 of the angiotensin II). On ceasing the angiotensin II, all variables recovered to baseline. In contrast, RSNA did not change in SAD rabbits with the angiotensin II infusion (RSNA was 98±8% of baseline on day 2 and 98±8% on day 6 of the angiotensin II infusion). These results support our hypothesis that the reduction in RSNA in response to a pressor dose of angiotensin II is dependent on an intact arterial baroreflex pathway.
Revised on February 8, 2005
Baroreceptor Denervation Prevents Sympathoinhibition During Angiotensin II-Induced Hypertension
Carolyn J. Barrett*;
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