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Arterial baroreflex control of muscle sympathetic nerve activity under orthostatic stress in humans

The mechanisms by which blood pressure is maintained against the orthostatic stress caused by gravity's effect on the fluid distribution within the body are important issues in physiology, especially in humans who usually adopt an upright posture. Peripheral vasoconstriction and increased heart...

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Autores principales: Ichinose, Masashi, Nishiyasu, Takeshi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3429084/
https://www.ncbi.nlm.nih.gov/pubmed/22934064
http://dx.doi.org/10.3389/fphys.2012.00314
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author Ichinose, Masashi
Nishiyasu, Takeshi
author_facet Ichinose, Masashi
Nishiyasu, Takeshi
author_sort Ichinose, Masashi
collection PubMed
description The mechanisms by which blood pressure is maintained against the orthostatic stress caused by gravity's effect on the fluid distribution within the body are important issues in physiology, especially in humans who usually adopt an upright posture. Peripheral vasoconstriction and increased heart rate (HR) are major cardiovascular adjustments to orthostatic stress and comprise part of the reflex response elicited via the carotid sinus and aortic baroreceptors (arterial baroreflex: ABR) and cardiopulmonary stretch receptors (cardiopulmonary baroreflex). In a series of studies, we have been characterizing the ABR-mediated regulation of cardiovascular hemodynamics and muscle sympathetic nerve activity (MSNA) while applying orthostatic stress in humans. We have found that under orthostatic stress, dynamic carotid baroreflex responses are modulated as exemplified by the increases in the MSNA, blood pressure, and HR responses elicited by carotid baroreflex unloading and the shorter period of MSNA suppression, comparable reduction and faster recovery of mean arterial blood pressure (MAP) and greater HR response to carotid baroreflex stimulation. Our results also show that ABR-mediated beat-to-beat control over burst incidence, burst strength and total MSNA is progressively modulated as orthostatic stress is increased until induction of syncope, and that the sensitivity of ABR control over the aforementioned MSNA variables is substantially reduced during the development of syncope. We suggest that in humans, the modulation of ABR function under orthostatic stress may be one of the mechanisms by which blood pressure is maintained and orthostatic hypotension limited, and impairment of ABR control over sympathetic vasomotor activity leads to the severe hypotension associated with orthostatic syncope.
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spelling pubmed-34290842012-08-29 Arterial baroreflex control of muscle sympathetic nerve activity under orthostatic stress in humans Ichinose, Masashi Nishiyasu, Takeshi Front Physiol Physiology The mechanisms by which blood pressure is maintained against the orthostatic stress caused by gravity's effect on the fluid distribution within the body are important issues in physiology, especially in humans who usually adopt an upright posture. Peripheral vasoconstriction and increased heart rate (HR) are major cardiovascular adjustments to orthostatic stress and comprise part of the reflex response elicited via the carotid sinus and aortic baroreceptors (arterial baroreflex: ABR) and cardiopulmonary stretch receptors (cardiopulmonary baroreflex). In a series of studies, we have been characterizing the ABR-mediated regulation of cardiovascular hemodynamics and muscle sympathetic nerve activity (MSNA) while applying orthostatic stress in humans. We have found that under orthostatic stress, dynamic carotid baroreflex responses are modulated as exemplified by the increases in the MSNA, blood pressure, and HR responses elicited by carotid baroreflex unloading and the shorter period of MSNA suppression, comparable reduction and faster recovery of mean arterial blood pressure (MAP) and greater HR response to carotid baroreflex stimulation. Our results also show that ABR-mediated beat-to-beat control over burst incidence, burst strength and total MSNA is progressively modulated as orthostatic stress is increased until induction of syncope, and that the sensitivity of ABR control over the aforementioned MSNA variables is substantially reduced during the development of syncope. We suggest that in humans, the modulation of ABR function under orthostatic stress may be one of the mechanisms by which blood pressure is maintained and orthostatic hypotension limited, and impairment of ABR control over sympathetic vasomotor activity leads to the severe hypotension associated with orthostatic syncope. Frontiers Media S.A. 2012-08-07 /pmc/articles/PMC3429084/ /pubmed/22934064 http://dx.doi.org/10.3389/fphys.2012.00314 Text en Copyright © 2012 Ichinose and Nishiyasu. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.
spellingShingle Physiology
Ichinose, Masashi
Nishiyasu, Takeshi
Arterial baroreflex control of muscle sympathetic nerve activity under orthostatic stress in humans
title Arterial baroreflex control of muscle sympathetic nerve activity under orthostatic stress in humans
title_full Arterial baroreflex control of muscle sympathetic nerve activity under orthostatic stress in humans
title_fullStr Arterial baroreflex control of muscle sympathetic nerve activity under orthostatic stress in humans
title_full_unstemmed Arterial baroreflex control of muscle sympathetic nerve activity under orthostatic stress in humans
title_short Arterial baroreflex control of muscle sympathetic nerve activity under orthostatic stress in humans
title_sort arterial baroreflex control of muscle sympathetic nerve activity under orthostatic stress in humans
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3429084/
https://www.ncbi.nlm.nih.gov/pubmed/22934064
http://dx.doi.org/10.3389/fphys.2012.00314
work_keys_str_mv AT ichinosemasashi arterialbaroreflexcontrolofmusclesympatheticnerveactivityunderorthostaticstressinhumans
AT nishiyasutakeshi arterialbaroreflexcontrolofmusclesympatheticnerveactivityunderorthostaticstressinhumans