Dual control of the vestibulosympathetic reflex following hypotension in rats.
10.4196/kjpp.2017.21.6.675
- Author:
Sang Eon PARK
1
;
Yuan Zhe JIN
;
Byung Rim PARK
Author Information
1. Department of Orthopedic Surgery, Kyung Hee University Hospital, Seoul 02447, Korea.
- Publication Type:Original Article
- Keywords:
Epinephrine;
Glutamate;
Intermediolateral cell column;
Orthostatic hypotension;
pERK;
Vestibulosympathetic reflex
- MeSH:
6-Cyano-7-nitroquinoxaline-2,3-dione;
Adrenal Medulla;
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid;
Animals;
Blood Pressure;
Denervation;
Dizocilpine Maleate;
Dizziness;
Epinephrine;
Excitatory Amino Acid Antagonists;
Glutamic Acid;
Headache;
Hypotension*;
Hypotension, Orthostatic;
Incidence;
N-Methylaspartate;
Nitroprusside;
Rats*;
Receptors, Glutamate;
Reflex*;
Spinal Cord Lateral Horn;
Syncope;
Vestibular Nuclei
- From:The Korean Journal of Physiology and Pharmacology
2017;21(6):675-686
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
