Because Lohmeier et al hypothesized that neurally induced suppression of renin secretion plays an important role in preventing pressure-dependent renin release during prolonged stimulation of the carotid sinus, they also sug-gested that this response plays an important role in permit- ting chronic reductions in arterial pressure during aroreflex activation. More specifically, they suggested that if the RAS were activated concomitantly with the fall in arterial pressure induced by stimulation of the carotid sinus, this would significantly attenuate the BP-lowering effects of baroreflex activation. To test this hypothesis, the baroreflex was activated for 7 days in dogs with hypertension induced by chronic infusion of angiotensin II.26 The infusion rate of angiotensin used in this study increased MAP w35 mm Hg and is associated with only a three-fold increase in circulating levels of the peptide. In this model of hypertension, there was a marked reduction ( w75%) in the BP-lowering effects of the baroreflex activation. Presumably, this study emphasizes the importance of renal sympathoinhibition in suppressing renin secretion and offsetting pressure-dependent renin release, which otherwise would greatly diminish increments in renal excretory function and attendant reductions in BP during carotid baroreflex ac
tivation. In addition, contribution from other aspects of sym
pathetic system might also play a role in this process.
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