B�tzinger neurons project towards bulbospinal neurons in the rostral ventrolateral medulla of the rat

Sun, Qi; Minson, Jane B; Llewellyn‐Smith, Ida J.; Arnolda, Leonard F; Chalmers, John; Pilowsky, Paul M.

doi:10.1002/(sici)1096-9861(19971110)388:1<23::aid-cne2>3.0.co;2-q

Cited by 53 publications

(57 citation statements)

References 37 publications

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“…Respiratory neurons in the ventral respiratory column are likely to provide inputs to nearby cardiovascular neurons (35,48). Neurons in the CVLM are governed by respiratory inputs, as well as excitatory inputs from the NTS, the caudal pressor area (CPA), and possibly other unknown inputs (25, 31, 40).…”

Section: Discussionmentioning

confidence: 99%

Catestatin, a chromogranin A-derived peptide, is sympathoinhibitory and attenuates sympathetic barosensitivity and the chemoreflex in rat CVLM

Gaede

Pilowsky

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Gaede AH, Pilowsky PM. Catestatin, a chromogranin A-derived peptide, is sympathoinhibitory and attenuates sympathetic barosensitivity and the chemoreflex in rat CVLM. Am J Physiol Regul Integr Comp Physiol 302: R365-R372, 2012. First published November 30, 2011 doi:10.1152/ajpregu.00409.2011.-Hypertension is a major cause of morbidity. The neuropeptide catestatin [human chromogranin A-(352-372)] is a peptide product of the vesicular protein chromogranin A. Studies in the periphery and in vitro studies show that catestatin blocks nicotine-stimulated catecholamine release and interacts with ␤-adrenoceptors and histamine receptors. Catestatin immunoreactivity is present in the rostral ventrolateral medulla (RVLM), a key site for blood pressure control in the brain stem. Recently, we reported that microinjection of catestatin into the RVLM is sympathoexcitatory and increases barosensitivity. Here, we report the effects of microinjection of catestatin (1 mM, 50 nl) into the caudal ventrolateral medulla (CVLM) in urethane-anesthetized, bilaterally vagotomized, artificially ventilated Sprague-Dawley rats (n ϭ 8). We recorded resting arterial pressure, splanchnic sympathetic nerve activity, phrenic nerve activity, heart rate, and measured cardiovascular homeostatic reflexes. Homeostatic reflexes were evaluated by measuring cardiovascular responses to carotid baroreceptor and peripheral chemoreceptor activation. Catestatin decreased basal levels of arterial pressure (Ϫ23 Ϯ 4 mmHg), sympathetic nerve activity (-26.6 Ϯ 5.7%), heart rate (Ϫ19 Ϯ 5 bpm), and phrenic nerve amplitude (Ϫ16.8 Ϯ 3.3%). Catestatin caused a 15% decrease in phrenic inspiratory period (T i) and a 16% increase in phrenic expiratory period (Te) but had no net effect on the phrenic interburst interval (Ttot). Catestatin decreased sympathetic barosensitivity by 63.6% and attenuated the peripheral chemoreflex (sympathetic nerve response to brief hypoxia; range decreased 39.9%; slope decreased 30.1%). The results suggest that catestatin plays an important role in central cardiorespiratory control. hypertension; hypoxic chemoreflex; neuropeptides; neuropharmacology SYMPATHETIC TONE, AND THE INTEGRATION of adaptive reflexes, is dependent on bulbospinal presympathetic excitatory neurons in the rostral ventrolateral medulla oblongata (RVLM). Presympathetic sympathoexcitatory neurons integrate information from the center and periphery (7).Chromogranin A (CgA) is packaged into large dense core secretory vesicles in nerve terminals throughout the peripheral and central nervous systems (45), but the function of this protein remains unclear. CgA is the precursor of several biologically active peptides that may play an important autocrine regulatory role in the neuroendocrine system (1, 12). One such cleavage product of CgA, catestatin, was first isolated from bovine adrenal medullary chromaffin cells, and, initially, it was shown to act as a potent noncompetitive nicotinic acetylcholine receptor (nAChR) antagonist (24), and a ␤-adrenoceptor agonist in peripheral ...

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Section: Discussionmentioning

confidence: 99%

Catestatin, a chromogranin A-derived peptide, is sympathoinhibitory and attenuates sympathetic barosensitivity and the chemoreflex in rat CVLM

Gaede

Pilowsky

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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“…RVLM presympathetic neurons receive a direct input from respiratory neurons (Sun et al, 1997), and their discharge is synchronous with different phases of PNA (Haselton and Guyenet, 1989;Miyawaki et al, 1995Miyawaki et al, , 1996Pilowsky et al, 1996). It has also been reported that at baseline SSNA has two distinct respiratory-related peaks, whereas LSNA has only one peak, i.e., during the PI period (Miyawaki et al, 2002).…”

Section: Cardiorespiratory Effects Of Nmu In Rvlm 219mentioning

confidence: 91%

“…The RVLM is a functionally heterogeneous region with cardiovascular and respiratory (Bö tzinger and pre-Bö tzinger) regions intermingled (Pilowsky et al, 1990(Pilowsky et al, , 2009Kanjhan et al, 1995). This close relationship, and synaptic input from respiratory neurons to RVLM neurons (Sun et al, 1997), along with close appositions between bulbospinal tyrosine hydroxylase-immunoreactive neurons of the C1 cell group and boutons from identified Bö tzinger neurons (Sun et al, 1994) suggest a possible site of action for the known interactions between the two systems and a possible explanation for the effects of NMU on respiration observed in this study.…”

Section: Cardiorespiratory Effects Of Nmu In Rvlm 219mentioning

confidence: 94%

Differential Cardiorespiratory and Sympathetic Reflex Responses to Microinjection of Neuromedin U in Rat Rostral Ventrolateral Medulla

Rahman

Shahid

Pilowsky

2012

J Pharmacol Exp Ther

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The rostral ventrolateral medulla (RVLM) regulates sympathetic vasomotor outflow and reflexes. Intracerebroventricular neuromedin U (NMU) increases sympathetic nerve activity (SNA), mean arterial pressure (MAP), and heart rate (HR), but the central nuclei that mediate these effects are unknown. In urethane-anesthetized, vagotomized, and artificially ventilated male Sprague-Dawley rats (n ϭ 36) the effects of bilateral microinjection of NMU (50 nl, each side) into RVLM on cardiorespiratory variables, somatosympathetic reflex, arterial baroreflex, and chemoreflex were investigated. Microinjection of NMU into RVLM elicited a hypertension, tachycardia, and an increase in splanchnic SNA (SSNA) and lumbar SNA (LSNA) at lower doses (25 and 50 pmol). At higher dose (100 pmol), NMU caused a biphasic response, a brief hypertension and sympathoexcitation followed by prolonged hypotension and sympathoinhibition. The peak excitatory and inhibitory response was found at 100 pmol NMU with an increase in MAP, HR, SSNA, and LSNA of 36 mm Hg, 20 beats per minute, 34%, and 89%, respectively, and a decrease of 33 mm Hg, 25 beats per minute, 42%, and 52%, respectively, from baseline. NMU, in the RVLM, also increased phrenic nerve amplitude and the expiratory period and reduced the inspiratory period. NMU (100 pmol) attenuated the somatosympathetic reflex and the sympathoexcitatory and respiratory responses to hypoxia and hypercapnia. After NMU injection in RVLM, the maximum gain of the SSNA baroreflex function curve was increased, but that of the LSNA was reduced. The present study provides functional evidence for a complex differential modulatory activity of NMU on the cardiovascular and reflex responses that are integrated in the RVLM.

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“…The respiratory system and sympathetic nervous system are anatomically linked in the brainstem [19][20][21][22]. Catecholinergic neurons have been shown to be phase-locked with the respiratory cycle [23].…”

Section: Body Stress and Sympathetic Activity As Factors Affecting Glmentioning

confidence: 99%

Review: Can Yoga Breathing Exercises Improve Glycemic Response and Insulin Sensitivity?

Wilson¹,

Kelly²,

Baker³

2017

J Yoga Phys Ther

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This is the first review of the literature on the effects of slow breathing on glycemic regulation and insulin sensitivity. While many studies have investigated the effects of yoga on individuals with diabetes, few studies have specifically focusing on the isolation of slow breathing as the principle factor in their intervention. While it is difficult to separate the exercise-related effects of yoga, there is considerable evidence that a breathing intervention is capable of increasing insulin sensitivity and improving glycemic regulation. This appears to be true both acutely and chronically in healthy individuals and those with diabetes. Yoga pranayama and the slow breathing practices that are fundamental to yoga represent a relatively low-cost and under-utilized intervention for individuals with conditions related to altered glycemic regulation and insulin sensitivity. More studies should focus on pranayama and slow breathing maneuvers to better clarify the role of respiratory modulation on glucose metabolism and insulin response.

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B�tzinger neurons project towards bulbospinal neurons in the rostral ventrolateral medulla of the rat

Cited by 53 publications

References 37 publications

Catestatin, a chromogranin A-derived peptide, is sympathoinhibitory and attenuates sympathetic barosensitivity and the chemoreflex in rat CVLM

Catestatin, a chromogranin A-derived peptide, is sympathoinhibitory and attenuates sympathetic barosensitivity and the chemoreflex in rat CVLM

Differential Cardiorespiratory and Sympathetic Reflex Responses to Microinjection of Neuromedin U in Rat Rostral Ventrolateral Medulla

Review: Can Yoga Breathing Exercises Improve Glycemic Response and Insulin Sensitivity?

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