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Arterial baroreceptor reflex control of renal sympathetic nerve activity (RSNA) has been proposed to play a role in long-term control of arterial pressure. The hypothesis that the ‘set point’ of the acute RSNA baroreflex curve determines the long-term level of arterial pressure is presented and challenged. Contrary to the hypothesis, studies on the long-term effects of sinoaortic denervation (SAD) on arterial pressure and RSNA, as well as more recent studies of chronic baroreceptor ‘unloading’ on arterial pressure, suggest that the basal levels of sympathetic nerve activity and arterial pressure are regulated independent of arterial baroreceptor input to the brainstem. Studies of the effect of SAD on the long-term salt sensitivity of arterial pressure are consistent with a short-term role, rather than a long-term role for the arterial baroreceptor reflex in regulation of arterial pressure during changes in dietary salt intake. Renal denervation studies suggest that renal nerves contribute to maintenance of the basal levels of arterial pressure. However, evidence that baroreflex control of the kidney plays a role in the maintenance of arterial pressure during changes in dietary salt intake is lacking. It is proposed that a ‘baroreflex-independent’ sympathetic control system must exist for the long-term regulation of sympathetic nerve activity and arterial pressure. The concept of a central nervous system ‘set point’ for long-term control of mean arterial pressure (CNS-MAP set point), and its involvement in the pathogenesis of hypertension, is discussed. [ABSTRACT FROM AUTHOR]

While there is no disputing the critical role of baroreflexes in buffering rapid changes in arterial pressure, their role in long-term pressure control has become an area of controversy. Recent experiments using novel techniques have challenged the traditional view that arterial baroreflexes are not involved in setting chronic arterial pressure levels. Resetting of the arterial baroreflex, often used as an argument against the arterial baroreflex playing a role in long-term pressure control is rarely complete. The arterial baroreflex is just one of the many neural, hormonal, and intrinsic mechanisms involved in arterial pressure control and while the removal of the arterial baroreflex alone has little effect on mean arterial pressure it is too simplistic to suggest that the baroreflex has no role in long-term pressure control. Renal sympathetic nerve activity appears to be particularly resistant to resetting in response to ANG H-induced hypertension. Given the important role of the kidneys in long-term pressure control, we suggest there is a clear need to develop experimental techniques whereby sympathetic nerve activity to the kidneys and other organs can be monitored over periods of weeks to months. [ABSTRACT FROM AUTHOR]

Recent findings in chronically instrumented animals challenge the classic concept that baroreflexes do not play a role in the chronic regulation of arterial pressure. As alterations in renal excretory function are of paramount importance in the chronic regulation of arterial pressure, several of these recent studies have focused on the long-term interactions between the baroreflex and the kidneys during chronic perturbations in arterial pressure and body fluid volumes. An emerging body of evidence indicates that the baroreflex is chronically activated in several experimental models of hypertension, but in most cases, the duration of these studies has not exceeded 2 wk. Although these studies suggest that the baroreflex may play a compensatory role in attenuating the severity of the hypertension, possibly even in primary hypertension with uncertain causes of sympathetic activation, there has been only limited assessment of the quantitative importance of this interaction in the regulation of arterial pressure. In experimental models of secondary hypertension, baroreflex suppression of renal sympathetic nerve activity is sustained and chronically promotes sodium excretion. This raises the possibility that the renal nerves may be the critical efferent link for baroreceptor-induced suppression of central sympathetic output through which long-term compensatory reductions in arterial pressure are produced. This contention is supported by strong theoretical evidence but must be corroborated by experimental studies. Finally, although it is now clear that pressure-induced increases in baroreflex activity persist for longer periods of time than previously suggested, studies using new tools and novel approaches and extending beyond 2 wk of hypertension are needed to elucidate the true role of the baroreflex in the pathogenesis of clinical hypertension. [ABSTRACT FROM AUTHOR]

Whether arterial baroreceptors play a role in setting the long-term level of mean arterial pressure (MAP) has been debated for more than 75 years. Because baroreceptor input is reciprocally related to efferent sympathetic nerve activity (SNA), it is obvious that baroreceptor unloading would cause an increase in MAP. Experimental proof of concept is evident acutely after baroreceptor denervation. Chronically, however, baroreceptor denervation is associated with highly variable changes in MAP but not sustained hypertension. The ability of baroreceptors to buffer imposed increases in MAP appears limited by a process termed ‘resetting,’ in which the threshold to fire shifts in the direction of the pressure change and if the pressure elevation is maintained, it leads to a rightward shift in the relationship between baroreceptor firing and MAP. The most common hypothesis linking baroreceptors to changes in MAP proposes that reduced vascular distensibility in baroreceptive areas would cause reduced firing at the same pulsatile pressure and, thus, reflexively increase SNA. This review focuses on effects of baroreceptor denervation in the regulation of MAP in human subjects compared with animal studies; the relationship between vascular compliance, MAP, and baroreceptor resetting; and, finally, the effect of chronic baroreceptor unloading on the regulation of MAP. [ABSTRACT FROM AUTHOR]

Examines the role of baroreceptors in the long-term control of arterial pressure. Occurrence of the changes in arterial pressure; Alterations of the average level of arterial pressure of an unstressed individual at rest; Decrease in plasma norepinephrine concentration that presumably reflects a decrease in sympathetic activity.

Stocker, Sean D., Jennifer C. Schiltz, and Alan F. Sved. Acute increases in arterial blood pressure do not reduce plasma vasopressin levels stimulated by angiotensin II or hyperosmolality in rats. Am J Physiol Regul Integr Comp Physiol 287: R127-R137, 2004. First published February 26, 2004; 10.1152/ajpregu.00526.2003.--The present study sought to determine whether an acute increase in arterial blood pressure (ABP) reduces plasma vasopressin (VP) levels stim- ulated by ANG II or hyperosmolality. During an intravenous infusion of ANG II (100 ng·kg-1·min-1), attenuation of the ANG II-evoked increase in ABP with diazoxide or minoxidil did not further enhance plasma VP levels in rats. When VP secretion was stimulated by an infusion of hypertonic saline, coinfusion of the α-adrenergic agonist phenylephrine (PE) significantly increased ABP but did not reduce plasma VP levels. In fact, plasma VP levels were enhanced. The enhancement of plasma VP levels cannot be explained by a direct stimulatory action of PE, as plasma VP levels of isosmotic rats did not change during a similar infusion of PE. An infusion of endothelin-1 in hyperosmotic rats significantly raised ABP but did not reduce plasma VP levels; rather, VP levels increased as observed with PE. In α-chloralose-anesthetized rats infused with hypertonic saline, inflation of an aortic cuff to increase ABP and stimulate arterial baroreceptors did not reduce plasma VP levels. In each experiment, plasma oxytocin levels paralleled plasma VP levels. Collectively, the present findings suggest that an acute increase in ABP does not inhibit VP secretion. baroreceptor; vasopressin; oxytocin [ABSTRACT FROM AUTHOR]