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Dual control of the vestibulosympathetic reflex following hypotension in rats
Orthostatic hypotension (OH) is associated with symptoms including headache, dizziness, and syncope. The incidence of OH increases with age. Attenuation of the vestibulosympathetic reflex (VSR) is also associated with an increased incidence of OH. In order to understand the pathophysiology of OH, we...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Physiological Society and The Korean Society of Pharmacology
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5709485/ https://www.ncbi.nlm.nih.gov/pubmed/29200911 http://dx.doi.org/10.4196/kjpp.2017.21.6.675 |
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author | Park, Sang Eon Jin, Yuan-Zhe Park, Byung Rim |
author_facet | Park, Sang Eon Jin, Yuan-Zhe Park, Byung Rim |
author_sort | Park, Sang Eon |
collection | PubMed |
description | Orthostatic hypotension (OH) is associated with symptoms including headache, dizziness, and syncope. The incidence of OH increases with age. Attenuation of the vestibulosympathetic reflex (VSR) is also associated with an increased incidence of OH. In order to understand the pathophysiology of OH, we investigated the physiological characteristics of the VSR in the disorder. We applied sodium nitroprusside (SNP) to conscious rats with sinoaortic denervation in order to induce hypotension. Expression of pERK in the intermediolateral cell column (IMC) of the T4~7 thoracic spinal regions, blood epinephrine levels, and blood pressure were evaluated following the administration of glutamate and/or SNP. SNP-induced hypotension led to increased pERK expression in the medial vestibular nucleus (MVN), rostral ventrolateral medullary nucleus (RVLM) and the IMC, as well as increased blood epinephrine levels. We co-administered either a glutamate receptor agonist or a glutamate receptor antagonist to the MVN or the RVLM. The administration of the glutamate receptor agonists, AMPA or NMDA, to the MVN or RVLM led to elevated blood pressure, increased pERK expression in the IMC, and increased blood epinephrine levels. Administration of the glutamate receptor antagonists, CNQX or MK801, to the MVN or RVLM attenuated the increased pERK expression and blood epinephrine levels caused by SNP-induced hypotension. These results suggest that two components of the pathway which maintains blood pressure are involved in the VSR induced by SNP. These are the neurogenic control of blood pressure via the RVLM and the humoral control of blood pressure via epinephrine release from the adrenal medulla. |
format | Online Article Text |
id | pubmed-5709485 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | The Korean Physiological Society and The Korean Society of Pharmacology |
record_format | MEDLINE/PubMed |
spelling | pubmed-57094852017-12-03 Dual control of the vestibulosympathetic reflex following hypotension in rats Park, Sang Eon Jin, Yuan-Zhe Park, Byung Rim Korean J Physiol Pharmacol Original Article Orthostatic hypotension (OH) is associated with symptoms including headache, dizziness, and syncope. The incidence of OH increases with age. Attenuation of the vestibulosympathetic reflex (VSR) is also associated with an increased incidence of OH. In order to understand the pathophysiology of OH, we investigated the physiological characteristics of the VSR in the disorder. We applied sodium nitroprusside (SNP) to conscious rats with sinoaortic denervation in order to induce hypotension. Expression of pERK in the intermediolateral cell column (IMC) of the T4~7 thoracic spinal regions, blood epinephrine levels, and blood pressure were evaluated following the administration of glutamate and/or SNP. SNP-induced hypotension led to increased pERK expression in the medial vestibular nucleus (MVN), rostral ventrolateral medullary nucleus (RVLM) and the IMC, as well as increased blood epinephrine levels. We co-administered either a glutamate receptor agonist or a glutamate receptor antagonist to the MVN or the RVLM. The administration of the glutamate receptor agonists, AMPA or NMDA, to the MVN or RVLM led to elevated blood pressure, increased pERK expression in the IMC, and increased blood epinephrine levels. Administration of the glutamate receptor antagonists, CNQX or MK801, to the MVN or RVLM attenuated the increased pERK expression and blood epinephrine levels caused by SNP-induced hypotension. These results suggest that two components of the pathway which maintains blood pressure are involved in the VSR induced by SNP. These are the neurogenic control of blood pressure via the RVLM and the humoral control of blood pressure via epinephrine release from the adrenal medulla. The Korean Physiological Society and The Korean Society of Pharmacology 2017-11 2017-10-30 /pmc/articles/PMC5709485/ /pubmed/29200911 http://dx.doi.org/10.4196/kjpp.2017.21.6.675 Text en Copyright © Korean J Physiol Pharmacol http://creativecommons.org/licenses/by-nc/4.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Park, Sang Eon Jin, Yuan-Zhe Park, Byung Rim Dual control of the vestibulosympathetic reflex following hypotension in rats |
title | Dual control of the vestibulosympathetic reflex following hypotension in rats |
title_full | Dual control of the vestibulosympathetic reflex following hypotension in rats |
title_fullStr | Dual control of the vestibulosympathetic reflex following hypotension in rats |
title_full_unstemmed | Dual control of the vestibulosympathetic reflex following hypotension in rats |
title_short | Dual control of the vestibulosympathetic reflex following hypotension in rats |
title_sort | dual control of the vestibulosympathetic reflex following hypotension in rats |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5709485/ https://www.ncbi.nlm.nih.gov/pubmed/29200911 http://dx.doi.org/10.4196/kjpp.2017.21.6.675 |
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