Introduction: Current consensus of baroreceptor function as important in short-term, but not in long-term control of blood pressure (BP) is challenged by recent studies applying newer experimental approaches. Methods: Evaluation of the literature published at Medline by search with key words: baroreflex, long-term control, blood pressure was undertaken. Results: McCubbin et al. demonstrated baroreceptors adapt or “reset” in response to maintained changes in pressure (hypotension/hypertension), which is completed within 48h. So, if baroreflex resetting is truly complete in chronic changes of BP, then the baroreflex could not possibly affect sympathetic activity. Cowley at al. demonstrated that sinaortic denervation (SAD) as well as carotid baroreceptor denervation causes a persistent decrease in vagal and sympathetic baroreflex sensitivity and an increase in BP variability ; however SAD do not lead to chronic hypertension. In contrast, Lohmeier et al. did an experiment with inervated (IK) and denervated kidney (DK). After infusion of angiotensin II., both kidneys were exposed to the same increase of mean arterial pressure and plasma Ang II concentration ; the only explanation for the increased sodium excretion in the IK is chronic suppression of renal sympathetic nerve activity (RSNA). After denervation of cardiopulmonary receptors and baroreceptors sodium excretion in the IK decreased during infusion of Ang II, suggesting that Ang II causes a sustained increase in RSNA. An increase activity would be predicted in response to activation of baroreceptors, if baroreceptors resetting is not complete during Ang II-induced hypertension. Conclusion: The examples above provide functional evidence that baroreceptor resetting in response to increased load may not always be complete. The most probable explanation is that the original concept that baroreceptor denervation is a model of chronic baroreceptor unloading, is most probably wrong.

Fundamental medical sciences