Arterial baroreceptor input contributes to long-term control of blood pressure.

A little more than three decades ago, there was little doubt that baroreceptors were crucial for both the short-term and long-term control of mean arterial blood pressure (MAP). Then, in 1970 it was reported that baroreceptors reset completely within 48 hours in hypertensive rats. Three years later, it was reported that MAP was near normal in dogs with both aortic and carotid baroreceptors denervated based on continuous measurements, thus discrediting numerous reports of denervation-induced hypertension. These two observations quickly led to a reevaluation of the importance of baroreceptor input in long-term control mechanisms. Finally, a consensus emerged that baroreceptor input could not be involved in long-term control of MAP, and this conclusion can be found in all modern textbooks of physiology used in the instruction of medical students. However, recent experimental observations have challenged the conclusion that baroreceptor input plays no role in the long-term control of MAP. In this article, the principal arguments against baroreceptor involvement in long-term control of MAP are summarized, and the new findings that suggest that a reappraisal of our current concept is required are reviewed.

Baroreceptors, baroreceptor unloading, and the long-term control of blood pressure.

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.

Effects of chronic baroreceptor unloading on blood pressure in the dog.

We have developed a new model of chronic baroreceptor unloading (CBU) in the dog. Initial characterization of the model indicated that CBU increased mean arterial pressure (MAP) by an average of 22 mmHg for 7 days. The goal of the present study was to replicate the previous study using telemetry to record MAP continuously and to determine the effects of CBU (n = 7) on chronic regulation of MAP. We also prepared a group of dogs with sinoaortic denervation (SAD, n = 6) to compare the time course of changes in MAP in the two models. Control levels (7 day average +/- SE) of MAP in the CBU and SAD groups were 94 +/- 2 and 94 +/- 1 mmHg, respectively. MAP averaged 124 +/- 8 and 103 +/- 4 mmHg during the first and second weeks after SAD (both P < 0.05) and then declined to levels not different from control during weeks 3-5. In the CBU group, MAP averaged 120 +/- 4 mmHg during the first week, declined to 111 +/- 4 mmHg during the second week, and stabilized at 104 mmHg during weeks 3-5 (all P < 0.05 compared with control). Plasma norepinephrine levels were increased significantly for the first week after SAD and for 2 wk after CBU but were not different from control for the remainder of the study. These results indicate that the initial increase in MAP after CBU is not sustained but declines to a level that is modestly higher than control. However, because MAP did not fall to control levels, the results are compatible with the hypothesis that baroreceptor input can influence the long-term level of MAP.

Baroreceptors and the long-term control of blood pressure.

The current consensus is that arterial baroreceptors are vitally important in the short term (seconds to minutes) control of mean arterial pressure (MAP) but are unimportant in determining the long-term level of MAP. The latter statement is based primarily on two observations: first, that baroreceptors rapidly reset to the prevailing level of MAP and second, that total baroreceptor denervation has no lasting effect on the average daily MAP, although the variability of MAP is increased dramatically. However, recent studies in intact experimental animals have produced results that suggest baroreceptor resetting may not be as rapid or complete as previously thought. Furthermore, reconsideration of the responses to baroreceptor denervation suggest that the condition may accurately represent responses to short-term baroreceptor unloading but not long-term unloading. Results obtained using a new model of chronic baroreceptor unloading indicate that the condition results in a sustained increase in MAP. These results strongly suggest that the role of baroreceptors in the long term control of MAP needs to be revisited.

Unloading arterial baroreceptors causes neurogenic hypertension.

We developed a new model to examine the role of arterial baroreceptors in the long-term control of mean arterial pressure (MAP) in dogs. Baroreceptors in the aortic arch and one carotid sinus were denervated, and catheters were implanted in the descending aorta and common carotid arteries. MAP and carotid sinus pressure (CSP) averaged 104 +/- 2 and 102 +/- 2 mmHg (means +/- 1 SE), respectively, during a 5-day control period. Baroreceptor unloading was induced by ligation of the common carotid artery proximal to the innervated sinus (n = 6 dogs). MAP and CSP averaged 127 +/- 7 and 100 +/- 3 mmHg, respectively, during the 7-day period of baroreceptor unloading. MAP was significantly elevated (P < 0.01) compared to control, but CSP was unchanged. Heart rate and plasma renin activity increased significantly in response to baroreceptor unloading. Removal of the ligature to restore normal flow through the carotid resulted in normalization of all variables. Ligation of the carotid below a denervated sinus (n = 4) caused a significant decrease in CSP but no systemic hypertension. These results indicate that chronic unloading of carotid baroreceptors can produce neurogenic hypertension and provide strong evidence that arterial baroreceptors are involved in the long-term control of blood pressure.