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Citation
Tags
HERO ID
3058113
Reference Type
Journal Article
Title
Increased rhythmicity in hypertensive arterial smooth muscle is linked to transient receptor potential canonical channels
Author(s)
Chen, X; Yang, D; Ma, S; He, H; Luo, Z; Feng, X; Cao, T; Ma, L; Yan, Z; Liu, D; Tepel, M; Zhu, Z
Year
2010
Is Peer Reviewed?
Yes
Journal
Journal of Cellular and Molecular Medicine
ISSN:
1582-1838
EISSN:
1582-4934
Volume
14
Issue
10
Page Numbers
2483-2494
PMID
19725917
DOI
10.1111/j.1582-4934.2009.00890.x
Web of Science Id
WOS:000283596400014
Abstract
Vasomotion describes oscillations of arterial vascular tone due to synchronized changes of intracellular calcium concentrations. Since increased calcium influx into vascular smooth muscle cells from spontaneously hypertensive rats (SHR) has been associated with variances of transient receptor potential canonical (TRPC) channels, in the present study we tested the hypothesis that increased vasomotion in hypertension is directly linked to increased TRPC expression. Using a small vessel myograph we observed significantly increased norepinephrine-induced vasomotion in mesenteric arterioles from SHR compared to normotensive Wistar-Kyoto (WKY) rats. Using immunoblottings we obtained significantly increased expression of TRPC1, TRPC3 and TRPC5 in mesenteric arterioles from SHR compared to WKY, whereas TRPC4 and TRPC6 showed no differences. Norepinephrine-induced vasomotion from SHR was significantly reduced in the presence of verapamil, SKF96365, 2-aminoethoxydiphenylborane (2-APB) or gadolinium. Pre-incubation of mesenteric arterioles with anti-TRPC1 and anti-TRPC3 antibodies significantly reduced norepinephrine-induced vasomotion and calcium influx. Control experiments with pre-incubation of TRPC antibodies plus their respective antigenic peptide or in the presence of anti-beta-actin antibodies or random immunoglobulins not related to TRPC channels showed no inhibitory effects of norepinephrine-induced vasomotion and calcium influx. Administration of candesartan or telmisartan, but not amlodipine to SHR for 16 weeks significantly reduced either the expression of TRPC1, TRPC3 and TRPC5 as well as norepinephrine-induced vasomotion in mesenteric arterioles. In conclusion we gave experimental evidence that the increased TRPC1, TRPC3 and TRPC5 expression in mesenteric arterioles from SHR causes increased vasomotion in hypertension.
Keywords
vasomotion; transient receptor potential channels; angiotensin II 1 receptor blocker; calcium channel blocker; hypertension
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