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Agmatine suppresses peripheral sympathetic tone by inhibiting N-type Ca(2+) channel activity via imidazoline I2 receptor activation

Authors
 Young-Hwan Kim  ;  Ji-Hyun Jeong  ;  Duck-Sun Ahn  ;  Seungsoo Chung 
Citation
 Biochemical and Biophysical Research Communications, Vol.477(3) : 406-412, 2016 
Journal Title
 Biochemical and Biophysical Research Communications 
ISSN
 0006-291X 
Issue Date
2016
MeSH
Action Potentials/drug effects ; Agmatine/pharmacology* ; Animals ; Calcium Channel Blockers/pharmacology* ; Calcium Channels, N-Type/drug effects* ; Electric Stimulation ; Imidazoline Receptors/agonists* ; In Vitro Techniques ; Male ; Mesenteric Arteries/drug effects ; Rats ; Rats, Sprague-Dawley ; Sympathetic Nervous System/drug effects*
Keywords
Agmatine ; Imidazoline receptor ; N-type calcium channel ; Sympathetic tone
Abstract
Agmatine, a putative endogenous ligand of imidazoline receptors, suppresses cardiovascular function by inhibiting peripheral sympathetic tone. However, the molecular identity of imidazoline receptor subtypes and its cellular mechanism underlying the agmatine-induced sympathetic suppression remains unknown. Meanwhile, N-type Ca(2+) channels are important for the regulation of NA release in the peripheral sympathetic nervous system. Therefore, it is possible that agmatine suppresses NA release in peripheral sympathetic nerve terminals by inhibiting Ca(2+) influx through N-type Ca(2+) channels. We tested this hypothesis by investigating agmatine effect on electrical field stimulation (EFS)-evoked contraction and NA release in endothelium-denuded rat superior mesenteric arterial strips. We also investigated the effect of agmatine on the N-type Ca(2+) current in superior cervical ganglion (SCG) neurons in rats. Our study demonstrates that agmatine suppresses peripheral sympathetic outflow via the imidazoline I2 receptor in rat mesenteric arteries. In addition, the agmatine-induced suppression of peripheral vascular sympathetic tone is mediated by modulating voltage-dependent N-type Ca(2+) channels in sympathetic nerve terminals. These results suggest a potential cellular mechanism for the agmatine-induced suppression of peripheral sympathetic tone. Furthermore, they provide basic and theoretical information regarding the development of new agents to treat hypertension.
Full Text
http://www.sciencedirect.com/science/article/pii/S0006291X1631004X
DOI
10.1016/j.bbrc.2016.06.086
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
김영환(Kim, Young Hwan)
안덕선(Ahn, Duk Sun) ORCID logo https://orcid.org/0000-0001-9351-6951
정승수(Chung, Seung Soo) ORCID logo https://orcid.org/0000-0002-3119-9628
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URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/152189
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