Sympathetic response to stimulation of the pontine A5 region in conscious rabbits

Maiorov, Dmitri N.; Wilton, Edwyn R; Badoer, Emilio; Petrie, D. R.; Head, Geoffrey A.; Malpas, Simon C.

doi:10.1016/s0006-8993(98)01150-0

Cited by 30 publications

(34 citation statements)

References 25 publications

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“…There is some evidence that adrenergic A5 neurons may act as chemosensors for CO 2 , since the activity of these cells is significantly increased by inspired CO 2 (42). In addition, stimulation of the A5 region with glutamate in conscious rabbits evokes a dose-dependent excitatory response in the renal SNA (50). Thus, based on the information described above, we could speculate that A5 noradrenergic neurons contribute to the activation of the sympathetic system and breathing by hypercapnia in rats.…”

Section: Role Of the Pontine Catecholaminergic System In Central Sympmentioning

confidence: 83%

Central chemoreceptors and neural mechanisms of cardiorespiratory control

Moreira

Takakura

Damasceno

et al. 2011

Braz J Med Biol Res

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The arterial partial pressure (P CO 2 ) of carbon dioxide is virtually constant because of the close match between the metabolic production of this gas and its excretion via breathing. Blood gas homeostasis does not rely solely on changes in lung ventilation, but also to a considerable extent on circulatory adjustments that regulate the transport of CO 2 from its sites of production to the lungs. The neural mechanisms that coordinate circulatory and ventilatory changes to achieve blood gas homeostasis are the subject of this review. Emphasis will be placed on the control of sympathetic outflow by central chemoreceptors. High levels of CO 2 exert an excitatory effect on sympathetic outflow that is mediated by specialized chemoreceptors such as the neurons located in the retrotrapezoid region. In addition, high CO 2 causes an aversive awareness in conscious animals, activating wakepromoting pathways such as the noradrenergic neurons. These neuronal groups, which may also be directly activated by brain acidification, have projections that contribute to the CO 2 -induced rise in breathing and sympathetic outflow. However, since the level of activity of the retrotrapezoid nucleus is regulated by converging inputs from wake-promoting systems, behavior-specific inputs from higher centers and by chemical drive, the main focus of the present manuscript is to review the contribution of central chemoreceptors to the control of autonomic and respiratory mechanisms.

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Section: Role Of the Pontine Catecholaminergic System In Central Sympmentioning

confidence: 83%

Central chemoreceptors and neural mechanisms of cardiorespiratory control

Moreira

Takakura

Damasceno

et al. 2011

Braz J Med Biol Res

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“…These fluctuations could have been caused by an arousal from sleep, as depicted in Fig. 1 or by the mechanical effects of increased ventilation on cardiac return, or perhaps by regional blood flow redistribution and differential activation of various sympathetic efferents (visceral ϾϾ skeletal muscle) caused by activation of the "A5 region" (46,52,73).…”

Section: Discussionmentioning

confidence: 99%

Selective optogenetic stimulation of the retrotrapezoid nucleus in sleeping rats activates breathing without changing blood pressure or causing arousal or sighs

Burke

Kanbar

Viar

et al. 2015

Journal of Applied Physiology

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Burke PG, Kanbar R, Viar KE, Stornetta RL, Guyenet PG. Selective optogenetic stimulation of the retrotrapezoid nucleus in sleeping rats activates breathing without changing blood pressure or causing arousal or sighs. J Appl Physiol 118: 1491-1501. First published April 9, 2015 doi:10.1152/japplphysiol.00164.2015.-Combined optogenetic activation of the retrotrapezoid nucleus (RTN; a CO 2/proton-activated brainstem nucleus) with nearby catecholaminergic neurons (C1 and A5), or selective C1 neuron stimulation, increases blood pressure (BP) and breathing, causes arousal from non-rapid eye movement (non-REM) sleep, and triggers sighs. Here we wished to determine which of these physiological responses are elicited when RTN neurons are selectively activated. The left rostral RTN and nearby A5 neurons were transduced with channelrhodopsin-2 (ChR2 ϩ ) using a lentiviral vector. Very few C1 cells were transduced. BP, breathing, EEG, and neck EMG were monitored. During non-REM sleep, photostimulation of ChR2 ϩ neurons (20s, 2-20 Hz) instantly increased V E without changing BP (13 rats). V E and BP were unaffected by light in nine control (ChR2 Ϫ ) rats. Photostimulation produced no sighs and caused arousal (EEG desynchronization) more frequently in ChR2 ϩ than ChR2 Ϫ rats (62 Ϯ 5% of trials vs. 25 Ϯ 2%; P Ͻ 0.0001). Six ChR2 ϩ rats then received spinal injections of a saporin-based toxin that spared RTN neurons but destroyed surrounding catecholaminergic neurons. Photostimulation of the ChR2 ϩ neurons produced the same ventilatory stimulation before and after lesion, but arousal was no longer elicited. Overall (all ChR2 ϩ rats combined), ⌬V E correlated with the number of ChR2 ϩ RTN neurons whereas arousal probability correlated with the number of ChR2 ϩ catecholaminergic neurons. In conclusion, RTN neurons activate breathing powerfully and, unlike the C1 cells, have minimal effects on BP and have a weak arousal capability at best. A5 neuron stimulation produces little effect on breathing and BP but does appear to facilitate arousal.arousal; A5 noradrenergic neurons; hypercapnia; non-REM sleep; retrotrapezoid nucleus HYPOXIA AND HYPERCAPNIA, ALONE or in combination, activate breathing and, if severe enough, produce arousal (17,60,62,63). The carotid bodies are largely responsible for the hypoxic ventilatory stimulation and for hypoxia-induced arousal because both responses are eliminated by ablating these organelles (17). How and where central nervous system (CNS) hypercarbia elicits the hypercapnic ventilatory reflex (HCVR) are still debated, and the CNS pathways responsible for arousal to hypoxia or hypercapnia are even more conjectural. The prevailing view is that both the HCVR and CO 2 -induced arousal result from the combined action of CO 2 on myriads of CNS pH-sensitive neurons, including serotonergic, noradrenergic, and orexinergic neurons (13,21,29,41,49,59,67).The retrotrapezoid nucleus (RTN) is a key structure for the HCVR. RTN neurons are glutamatergic and seem to operate both as a central respiratory chemorece...

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“…Ang II has long been described as sympathoexcitatory, acting within the central nervous system to increase SNA. Previous studies have demonstrated that the central administration of Ang II to a number of sites within the brain, including the area postrema, subfornical organ, pontine A5, 23 and paraventricular nucleus, 24,25 results in elevations in SNA. In addition, the expression of Ang II type I receptors in both the paraventricular nucleus and subfornical organs is higher after a 4-week subpressor infusion of Ang II in the rat.…”

Section: Guild Et Al Chronic Increased Rsna In Hypertension 617mentioning

confidence: 99%

High Dietary Salt and Angiotensin II Chronically Increase Renal Sympathetic Nerve Activity

et al. 2012

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Abstract-Overactivity of the sympathetic nervous system has long been implicated in the hypertensive response to elevated angiotensin II (Ang II) levels. Although recent studies suggest that high dietary salt may alter cardiovascular responses to Ang II, direct evidence demonstrating chronic activation of sympathetic nerve activity is lacking. The objective of this study was to determine whether a low dose of Ang II, on a background of high salt intake, would result in a chronic increase in renal sympathetic nerve activity (RSNA Key Words: sympathetic nervous system Ⅲ hypertension Ⅲ angiotensin II Ⅲ salt Ⅲ renal sympathetic nerve activity Ⅲ telemetry E levated sympathetic nerve activity (SNA), in particular to the kidneys and heart, and blunting of arterial baroreflexes are well-established hallmarks of hypertension. 1,2 Although a novel surgical approach of removing the renal nerves is showing initial promise in treating resistant hypertension, 3,4 it is clear that we need to better understand the long-term modulators of the level of renal SNA (RSNA). One potential regulator of SNA in hypertension is angiotensin II (Ang II). In addition to the actions of elevated Ang II in the periphery, to increase volume retention and total peripheral resistance, it has been proposed that Ang II acts via central nervous system pathways to increase SNA. 4,5 The ability of elevated Ang II to chronically increase SNA is highly controversial. Initially, using indirect methods to assess sympathetic tone, enhanced responses to ganglionic blockade 6,7 and a delayed development of hypertension in renal denervated animals 8,9 supported the involvement of an increase in SNA in animal models of Ang II-induced hypertension. However, sympathoexcitation is not a universal finding, with some studies indicating no change in nerve activity, both when nerve activity has been directly recorded 10 or assessed with ganglionic blockade. 11 Furthermore, in studies where Ang II caused an immediate increase in arterial pressure, a renal sympatho-inhibitory effect has been reported. 12-14 Specifically, we have shown, using direct recordings of RSNA in the rabbit, that, in response to a 7-day infusion of Ang II, there is a pronounced and sustained decrease in RSNA. 13 The dose of Ang II in that study was immediately pressor (50 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 IV), and the decrease in RSNA was eliminated in baroreceptor denervated animals, suggesting that the decrease in RSNA was baroreflex mediated.

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Sympathetic response to stimulation of the pontine A5 region in conscious rabbits

Cited by 30 publications

References 25 publications

Central chemoreceptors and neural mechanisms of cardiorespiratory control

Central chemoreceptors and neural mechanisms of cardiorespiratory control

Selective optogenetic stimulation of the retrotrapezoid nucleus in sleeping rats activates breathing without changing blood pressure or causing arousal or sighs

High Dietary Salt and Angiotensin II Chronically Increase Renal Sympathetic Nerve Activity

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