Baroreceptor denervation prevents sympathoinhibition during angiotensin II-induced hypertension

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 center dot kg(-1) center dot min(-1)). The arterial pressure responses in the 2 groups of rabbits were not significantly different ( 82 +/- 3 mm Hg sham versus 83 +/- 3 mmHg 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.