The Baroreceptor Reflex: Novel Methods and Mechanisms

Chapleau, Mark W.; Abboud, François M.

doi:10.1007/978-1-4419-9054-9_1

Cited by 9 publications

(8 citation statements)

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“…Over 10 years ago we first used aortic baroreceptor nodose neurones in culture to characterize mechanosensitive conductances and single channel units that were blocked by Gd 3+ (Hajduczok et al 1994; Cunningham et al 1995, 1997; Sharma et al 1995; Kraske et al 1998). We then found in these somata, and more importantly in their terminals, subunits of the DEG/ENaC superfamily of cationic, non‐voltage‐gated, non‐ligand‐gated, amiloride sensitive, mechanosensitive channels (Drummond et al 1998; Snitsarev et al 2002; Chapleau & Abboud, 2004). At present a subunit of the acid sensing ion channels subfamily (ASIC2) has been described as a mechanosensor in mammalian peripheral sensory nerve, and our preliminary work with genetic deletion of this subunit ASIC2 reveals a significant impairment of baroreceptor afferents and the baroreflex (Price et al 2000; Ma et al 2001 a ; Chapleau & Abboud, 2004).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, the presence of endothelium and vascular muscle along with mucosal and other cell types in the vascular wall make it difficult to attribute changes in baroreceptor (BR) or sensory nerve activity solely to direct actions on the nerve terminals. Factors released from nearby cells and changes in vascular smooth muscle tone can alter BR activity (Chapleau & Abboud, 2004). These limitations motivated us and others to develop an in vitro preparation of isolated nodose neurones in culture.…”

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Mechano‐ and chemosensitivity of rat nodose neurones – selective excitatory effects of prostacyclin

Snitsarev

Whiteis

Chapleau

et al. 2007

The Journal of Physiology

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Nodose ganglion sensory neurones exert a significant reflex autonomic influence. We contrasted their mechanosensitivity, excitability and chemosensitivity in response to the stable prostacyclin (PGI 2 ) analogue carbacyclin (cPGI) in culture. Under current clamp conditions we measured changes in membrane potential (ΔmV) and action potential (AP) responses to mechanically induced depolarizations and depolarizing current injections before and after superfusion of cPGI (1 μM and 10 μM). Chemosensitivity was indicated by augmentation of AP firing frequency and increased maximum gain of AP frequency (max. dAP/dΔmV), during superfusion with cPGI. Results indicate that two groups of neurones, A and B, are mechanosensitive (MS) and one group, C, is mechanoinsensitive (MI). Group A shows modest depolarization without AP generation during mechanical stimulation, and no increase in max. dAP/dΔmV, despite a marked increase in electrical depolarization with cPGI. Group B shows pronounced mechanical depolarization accompanied by enhanced AP discharge with cPGI, and an increase in max. dAP/dΔmV. Group C remains MI after cPGI but is more excitable and markedly chemosensitive (CS) with a pronounced enhancement of max. dAP/dΔmV with cPGI. The effect of cPGI on ionic conductances indicates that it does not sensitize the mechanically gated depolarizing degenerin/epithelial Na + channels (DEG/ENaC), but it inhibits two voltage-gated K + currents, Maxi-K and M-current, causing enhanced AP firing frequency and depolarization, respectively. We conclude that MS nodose neurones may be unimodal MS or bimodal MS/CS, and that MI neurones are unimodal CS, and much more CS to cPGI than MS/CS neurones. We suggest that the known excitatory effect of PGI 2 on baroreceptor and vagal afferent fibres is mediated by inhibition of voltage-gated K + channels (Maxi-K and M-current) and not by an effect on mechanically gated DEG/ENaC channels.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Mechano‐ and chemosensitivity of rat nodose neurones – selective excitatory effects of prostacyclin

Snitsarev

Whiteis

Chapleau

et al. 2007

The Journal of Physiology

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“…Mice are particularly useful mammalian models that are not only susceptible to genetic manipulation but can also be used in physiological, anatomical, cellular, and molecular studies (5,6). In the present study, we hypothesized that baroreflex control of the HR was reduced following CIH, and the reduction of vagal efferent control of the heart might account for the attenuated baroreflex sensitivity.…”

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confidence: 88%

Chronic intermittent hypoxia impairs baroreflex control of heart rate but enhances heart rate responses to vagal efferent stimulation in anesthetized mice

Lin¹,

Liu²,

Gozal³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Z. Chronic intermittent hypoxia impairs baroreflex control of heart rate but enhances heart rate responses to vagal efferent stimulation in anesthetized mice. Am J Physiol Heart Circ Physiol 293: H997-H1006, 2007. First published March 23, 2007; doi:10.1152/ajpheart.01124.2006.-Chronic intermittent hypoxia (CIH) leads to increased sympathetic nerve activity and arterial hypertension. In this study, we tested the hypothesis that CIH impairs baroreflex (BR) control of heart rate (HR) in mice, and that decreased cardiac chronotropic responsiveness to vagal efferent activity contributes to such impairment. C57BL/6J mice were exposed to either room air (RA) or CIH (6-min alternations of 21% O2 and 5.7% O2, 12 h/day) for 90 days. After the treatment period, mice were anesthetized (Avertin) and arterial blood pressure (ABP) was measured from the femoral artery. Mean ABP (MABP) was significantly increased in mice exposed to CIH (98.7 Ϯ 2.5 vs. RA: 78.9 Ϯ 1.4 mmHg, P Ͻ 0.001). CIH increased HR significantly (584.7 Ϯ 8.9 beats/min; RA: 518.2 Ϯ 17.9 beats/min, P Ͻ 0.05). Sustained infusion of phenylephrine (PE) at different doses (0.1-0.4 g/min) significantly increased MABP in both CIH and RA mice, but the ABP-mediated decreases in HR were significantly attenuated in mice exposed to CIH (P Ͻ 0.001). In contrast, decreases in HR in response to electrical stimulation of the left vagus nerve (30 A, 2-ms pulses) were significantly enhanced in mice exposed to CIH compared with RA mice at low frequencies. We conclude that CIH elicits a sustained impairment of baroreflex control of HR in mice. The blunted BR-mediated bradycardia occurs despite enhanced cardiac chronotropic responsiveness to vagal efferent stimulation. This suggests that an afferent and/or a central defect is responsible for the baroreflex impairment following CIH. nucleus ambiguus; obstructive sleep apnea; cardiac ganglia OBSTRUCTIVE SLEEP APNEA (OSA) is associated with substantial morbidities involving the central nervous system and cardiovascular systems (43, 50). Chronic intermittent hypoxia (CIH), which epitomizes one of the characteristics of OSA, has been used as a useful model for OSA (18,41). Regarding the latter, of particular physiological and clinical importance, is baroreflex control of heart rate (HR) (baroreflex sensitivity). Attenuation of baroreflex sensitivity is closely associated with several clinical conditions, including heart failure (16, 25, 44), and is considered as an independent risk factor for cardiac failure and sudden death (22). Therefore, an increased understanding of the physiological and anatomical characteristics of CIHassociated changes of the baroreflex pathways is clearly needed for improved formulation of interventional strategies aimed at reducing the morbidity associated with OSA.Previously, we demonstrated that baroreflex control of the HR was significantly reduced following CIH in Fisher 344 (F344) young adult rats (29). In addition, we showed that vagal cardiac motor neurons in the nucleus ambiguus projecting to cardiac...

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“…The NTS is important for central feedback regulation of BP control. One of the most potent regulatory feedback inputs into the NTS is the baroreflex (Chapleau and Abboud, 2004; Guyton, 1991). Changes in BP are immediately detected by aortic arch and carotid sinus baroreceptors, which then signal the information to the NTS, which processes these signals and modulates the synaptic output from RVLM through a relay involving the caudal ventrolateral medulla (Colombari et al, 2001; Dampney, 1994; Guyenet, 2006).…”

Section: Overview Of the Brain Control Of Blood Pressurementioning

confidence: 99%

A current view of brain renin–angiotensin system: Is the (pro)renin receptor the missing link?

Cuadra

Shan

Sumners

et al. 2010

Pharmacology & Therapeutics

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The renin angiotensin system (RAS) plays a central role in the brain to regulate blood pressure (BP). This role includes the modulation of sympathetic nerve activity (SNA) that regulates vascular tone, the regulation of secretion of neurohormones that have a critical role in electrolyte and fluid homeostasis, and by influencing behavioral processes to increase salt and water intake. Based on decades of research it is clear that angiotensin II (Ang II), the major bioactive product of the RAS, mediates these actions largely via its Ang II type 1 receptor (AT1R), located within hypothalamic and brainstem control centers. However, the mechanisms of brain RAS function have been questioned, due in large part to low expression levels of the rate limiting enzyme renin within the central nervous system. Tissue localized RAS has been observed in heart, kidney tubules and vascular cells. Studies have also given rise to the hypothesis for localized RAS function within the brain, so that Ang II can act in a paracrine manner to influence neuronal activity. The recently discovered (pro)renin receptor (PRR) may be key in this mechanism as it serves to sequester renin and prorenin for localized RAS activity. Thus, the PRR can potentially mitigate the low levels of renin expression in the brain to propagate Ang II action. In this review we examine the regulation, expression and functional properties of the various RAS components in the brain with particular focus on the different roles that PRR may have in BP regulation and hypertension.

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The Baroreceptor Reflex: Novel Methods and Mechanisms

Cited by 9 publications

References 125 publications

Mechano‐ and chemosensitivity of rat nodose neurones – selective excitatory effects of prostacyclin

Mechano‐ and chemosensitivity of rat nodose neurones – selective excitatory effects of prostacyclin

Chronic intermittent hypoxia impairs baroreflex control of heart rate but enhances heart rate responses to vagal efferent stimulation in anesthetized mice

A current view of brain renin–angiotensin system: Is the (pro)renin receptor the missing link?

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