ID | 55330 |
FullText URL | |
Author |
Tangsucharit, Panot
Department of Clinical Pharmaceutical Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Takatori, Shingo
Department of Clinical Pharmaceutical Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Zamami, Yoshito
Department of Pharmaceutical Care and Health Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Goda, Mitsuhiro
Department of Clinical Pharmaceutical Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Pakdeechote, Poungrat
Department of Physiology, Faculty of Medicine, Khon Kaen University
Kawasaki, Hiromu
Department of Clinical Pharmaceutical Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Takayama, Fusako
Department of Clinical Pharmaceutical Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
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Abstract | The present study investigated pharmacological characterizations of muscarinic acetylcholine receptor (AChR) subtypes involving ACh-induced endothelium-independent vasodilatation in rat mesenteric arteries. Changes in perfusion pressure to periarterial nerve stimulation and ACh were measured before and after the perfusion of Krebs solution containing muscarinic receptor antagonists. Distributions of muscarinic AChR subtypes in mesenteric arteries with an intact endothelium were studied using Western blotting. The expression level of M1 and M3 was significantly greater than that of M2. Endothelium removal significantly decreased expression levels of M2 and M3, but not M1. In perfused mesenteric vascular beds with intact endothelium and active tone, exogenous ACh (1, 10, and 100 nmol) produced concentration-dependent and long-lasting vasodilatations. In endothelium-denuded preparations, relaxation to ACh (1 nmol) disappeared, but ACh at 10 and 100 nmol caused long-lasting vasodilatations, which were markedly blocked by the treatment of pirenzepine (M1 antagonist) or 4-DAMP (M1 and M3 antagonist) plus hexamethonium (nicotinic AChR antagonist), but not methoctramine (M2 and M4 antagonist). These results suggest that muscarinic AChR subtypes, mainly M1, distribute throughout the rat mesenteric arteries, and that activation of M1 and/or M3 which may be located on CGRPergic nerves releases CGRP, causing an endothelium-independent vasodilatation.
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Keywords | Acetylcholine-induced vasodilatation
CGRPergic nerves
Muscarinic receptor subtypes
Rat mesenteric arteries
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Published Date | 2016-01
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Publication Title |
Journal of Pharmacological Sciences
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Volume | volume130
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Issue | issue1
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Publisher | Japanese Pharmacological Society
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Start Page | 24
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End Page | 32
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ISSN | 1347-8613
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NCID | AA11806667
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Content Type |
Journal Article
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language |
English
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OAI-PMH Set |
岡山大学
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Copyright Holders | https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
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File Version | publisher
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PubMed ID | |
DOI | |
Web of Science KeyUT | |
Related Url | https://doi.org/10.1016/j.jphs.2015.12.005
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