Acute resetting in two functionally different types of carotid baroreceptors.

Seagard, J. L.; Gallenberg, Lori A.; Hopp, Francis A.; Dean, Caron

doi:10.1161/01.res.70.3.559

Cited by 48 publications

(24 citation statements)

References 31 publications

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“…More importantly, it has been shown that type 1 receptors undergo acute resetting, whereas type 2 receptors do not. This difference has led to the hypothesis that type 1 receptors are involved in the second-tosecond stabilization of MAP and type 2 receptors are involved in signaling the absolute level of MAP (24). Unfortunately, there appear to be no studies that determined whether both type 1 and type 2 receptors adapt similarly during chronic states of altered MAP.…”

Section: Discussionmentioning

confidence: 99%

Effects of chronic baroreceptor unloading on blood pressure in the dog

Thrasher

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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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 ϭ 7) on chronic regulation of MAP. We also prepared a group of dogs with sinoaortic denervation (SAD, n ϭ 6) to compare the time course of changes in MAP in the two models. Control levels (7 day average Ϯ SE) of MAP in the CBU and SAD groups were 94 Ϯ 2 and 94 Ϯ 1 mmHg, respectively. MAP averaged 124 Ϯ 8 and 103 Ϯ 4 mmHg during the first and second weeks after SAD (both P Ͻ 0.05) and then declined to levels not different from control during weeks 3-5. In the CBU group, MAP averaged 120 Ϯ 4 mmHg during the first week, declined to 111 Ϯ 4 mmHg during the second week, and stabilized at 104 mmHg during weeks 3-5 (all P Ͻ 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 longterm level of MAP. neurogenic hypertension; arterial baroreceptors; plasma norepinephrine; renin; aldosterone THERE IS GENERAL AGREEMENT that arterial baroreceptors play a vital role in the short-term (seconds to minutes) stabilization of mean arterial pressure (MAP) (2, 5, 8). However, it is also well established that arterial baroreceptors play no role in setting the long-term level of MAP (2, 5, 8). The scientific basis for this conclusion has been succinctly reviewed by Cowley (5). The most compelling evidence that baroreceptors cannot be involved in the long-term regulation of MAP is that complete denervation of carotid sinus and aortic baroreceptors (SAD) has no long-term effect on the level of MAP (6,19,22) and that baroreceptors adapt to experimentally induced changes in MAP (12, 17). These observations provide the basis to argue that, because removal of baroreceptors has no effect on the level of MAP, something else must regulate MAP chronically and, if baroreceptors reset to the prevailing level of MAP over time, they cannot provide a chronic error signal to medullary circuits controlling sympathetic outflow.We have developed a new model of chronic baroreceptor unloading (CBU) in the dog that is based on the ligation of the carotid artery proximal to an innervated sinus with all other baroreceptor areas denervated (28). Initial experiments to characterize the model determined that systemic MAP increased significantly, averaging 22 Ϯ 2 mmHg above control over 7 days, whereas carotid sinus pressure (CSP) was not different from control levels, averaging Ϫ2 Ϯ 2 mmHg below control (28). These results appear at odds with the argume...

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Section: Discussionmentioning

confidence: 99%

Effects of chronic baroreceptor unloading on blood pressure in the dog

Thrasher

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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“…In addition, the receptors that display the phenomenon of rapid resetting appear to be associated with myelinated fibers (55). However, many of the baroreceptors communicate via unmyelinated axons, and these receptors appear to lack the property of rapid resetting (54). There is evidence that receptors with unmyelinated fibers do reset in models of chronic hypertension but not to the same extent as receptors with myelinated fibers (35).…”

Section: Baroreceptor Resettingmentioning

confidence: 99%

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

Thrasher¹

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Thrasher, Terry N. Baroreceptors, baroreceptor unloading, and the long-term control of blood pressure. Am J Physiol Regul Integr Comp Physiol 288: R819 -R827, 2005; doi:10.1152/ajpregu.00813.2004.-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.hypertension; sympathetic nerve activity THE SUSPICION THAT INCREASED sympathetic nerve activity (SNA) could play a role in the development of essential (i.e., primary) hypertension has been considered for a long time (24, 29, 37); however, definitive evidence that this suspicion is true has appeared only relatively recently. Increases in cardiac and renal norepinephrine spillover (an index of SNA to these organs) have been demonstrated in patients with borderline and mild essential hypertension (23). Moreover, direct measurements of muscle SNA via microneurography have indicated increased activity in subjects with essential hypertension (4, 67). The fact that increased SNA is detectable before established hypertension provides a known mechanism in the etiology of the condition; however, the cause of the increase in SNA is not known.It is generally agreed that essential hypertension arises from a combination of genetic and environmental influences (24). Thus the range of factors that could drive an increase in SNA is enormous. One of the best known and intensely studied of these factors is the reciprocal relationship between arterial baroreceptor input and sympathetic outflow. Experiments in the early part of the 20th century observed that denervation of baroreceptors in the carotid sinus and aortic arch (SAD) in experimental animals produced striking and highly variable increases in mean arterial pressure (MAP, see Ref. 29 for review of the early literature). However,...

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“…It has been proposed that the two types of fibers may act differentially, having different "purposes," allowing arterial pressure to be buffered over a wide operating range and both rapid and slow changes in arterial pressure to be buffered (84). Importantly, there is evidence that the two fiber types may differ in their ability to reset (69,85). It should also be noted that the typical methods for monitoring afferent baroreceptor activity, namely single or so-called whole nerve recordings, are biased toward A fibers with their larger spikes (1, 6), despite the fact that histological studies have shown that C fibers outnumber A fibers in baroreceptor nerves in both the rabbit (79) and rat (7).…”

Section: Possible Mechanisms Regulating the Long-term Level Of Sna: Amentioning

confidence: 99%

What sets the long-term level of sympathetic nerve activity: is there a role for arterial baroreceptors?

Malpas

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Malpas, Simon C. What sets the long-term level of sympathetic nerve activity: is there a role for arterial baroreceptors? Am J Physiol Regul Integr Comp Physiol 286: R1-R12, 2004; 10.1152/ajpregu.00496.2003.-Much of our knowledge of the influence of the sympathetic nervous system on the control of blood pressure is built on experimental approaches that focus very much on time scales Ͻ24 h. Although direct recordings of sympathetic nerve activity (SNA) over short time scales provide important information, it is difficult to place their relevance over the longer term where the development of chronic changes in blood pressure are likely to be a mixture of hormonal, renal, and neural influences. Recently new experimental approaches are now revealing a possible role for arterial baroreceptors in the chronic regulation of SNA. These studies reveal that chronic increases in blood pressure are associated with chronic changes in SNA that may be due to nonresetting of the blood pressure-SNA baroreflex relationship. This review discusses the implications of such information, highlighting new technologies for long-term recording of SNA that appear to hold much promise for revealing the role of SNA to the kidney for the long-term control of blood pressure. blood pressure; baroreflex; renal THE CONTROL OF ARTERIAL PRESSURE is a complex mixture of the long-and short-term influences of hormones, local vascular factors, and neural mechanisms. With regard to neural influences, much progress has been made in recent years on the central nervous system pathways involved in regulating sympathetic nerve activity (SNA) and the effect of that activity on vascular resistance. However, our knowledge of this control is mostly confined to short time scales of seconds and minutes, with a paucity of studies extending their focus to the longer term aspects (Ͼ24 h). Yet such information is liable to be critical in understanding the pathogenesis of hypertension where the onset of the disease is most likely to be a combination of slowly developing factors. As new tools for assessing sympathetic activity over longer time scales emerge, there is a growing desire and ability to understand longer term aspects of the regulation of SNA. It is recognized that pathways involved in regulating blood volume, osmolarity, and oxygen levels, as well as chronic changes in central nervous system function, are all likely to be important factors in understanding how SNA is controlled. However, given the revival in the hypothesis that arterial baroreflexes play a role in regulating the long-term levels of blood pressure, this review concentrates on the recent research supporting this concept. HISTORY

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Acute resetting in two functionally different types of carotid baroreceptors.

Cited by 48 publications

References 31 publications

Effects of chronic baroreceptor unloading on blood pressure in the dog

Effects of chronic baroreceptor unloading on blood pressure in the dog

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

What sets the long-term level of sympathetic nerve activity: is there a role for arterial baroreceptors?

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