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Protease-activated receptor 2 activation inhibits N-type Ca2+ currents in rat peripheral sympathetic neurons.

 Young Hwan Kim  ;  Duck Sun Ahn  ;  Myeong Ok Kim  ;  Ji Hyun Joeng  ;  Seungsoo Chung 
 MOLECULES AND CELLS, Vol.37(11) : 804-811, 2014 
Journal Title
Issue Date
Action Potentials/drug effects ; Animals ; Calcium Channels, N-Type/metabolism* ; Ganglia, Sympathetic/enzymology* ; Hypotension/metabolism* ; Male ; Mesenteric Arteries/physiology ; Neurons/metabolism ; Oligopeptides/pharmacology* ; Rats ; Rats, Sprague-Dawley ; Receptor, PAR-2/agonists ; Receptor, PAR-2/metabolism*
N-type Ca2+ channel ; celiac ganglion ; hypotension ; peripheral sympathetic output ; protease-activated receptor 2
The protease-activated receptor (PAR)-2 is highly expressed in endothelial cells and vascular smooth muscle cells. It plays a crucial role in regulating blood pressure via the modulation of peripheral vascular tone. Although several mechanisms have been suggested to explain PAR-2-induced hypotension, the precise mechanism remains to be elucidated. To investigate this possibility, we investigated the effects of PAR-2 activation on N-type Ca(2+) currents (I(Ca-N)) in isolated neurons of the celiac ganglion (CG), which is involved in the sympathetic regulation of mesenteric artery vascular tone. PAR-2 agonists irreversibly diminished voltage-gated Ca(2+) currents (I(Ca)), measured using the patch-clamp method, in rat CG neurons, whereas thrombin had little effect on I(Ca). This PAR-2-induced inhibition was almost completely prevented by ω-CgTx, a potent N-type Ca(2+) channel blocker, suggesting the involvement of N-type Ca(2+) channels in PAR-2-induced inhibition. In addition, PAR-2 agonists inhibited I(Ca-N) in a voltage-independent manner in rat CG neurons. Moreover, PAR-2 agonists reduced action potential (AP) firing frequency as measured using the current-clamp method in rat CG neurons. This inhibition of AP firing induced by PAR-2 agonists was almost completely prevented by ω-CgTx, indicating that PAR-2 activation may regulate the membrane excitability of peripheral sympathetic neurons through modulation of N-type Ca(2+) channels. In conclusion, the present findings demonstrate that the activation of PAR-2 suppresses peripheral sympathetic outflow by modulating N-type Ca(2+) channel activity, which appears to be involved in PAR-2-induced hypotension, in peripheral sympathetic nerve terminals.
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1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Young Hwan(김영환)
Ahn, Duk Sun(안덕선) ORCID logo https://orcid.org/0000-0001-9351-6951
Chung, Seung Soo(정승수) ORCID logo https://orcid.org/0000-0002-3119-9628
Joeng, Ji Hyun(정지현)
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