Increased transient receptor potential channel TRPC3 expression in spontaneously hypertensive rats

被引:72
作者
Liu, DY
Scholze, A
Zhu, ZM
Kreutz, R
Wehland-von-Trebra, M
Zidek, W
Tepel, M [1 ]
机构
[1] Med Klin 4, Nephrol Dept Hypertens & Endocrinol, Charite Campus Benjamin Franklin,Hindenburgdamm 3, D-12200 Berlin, Germany
[2] Third Mil Med Univ, Daping Hosp, Dept Hypertens & Endocrinol, Chongqing, Peoples R China
[3] Inst Klin Pharmakol & Toxikol, Berlin, Germany
基金
中国国家自然科学基金;
关键词
transient receptor potential channel; spontaneously hypertensive rats; calcium; siRNA;
D O I
10.1016/j.amjhyper.2005.05.033
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Background: Disturbances in the regulation of cytosolic calcium concentration have been attributed to primary hypertension, but the role of calcium-permeable transient receptor potential canonical channel 3 (TRPC3) has not yet been evaluated in primary hypertension. Methods: Expression of TRPC3 was determined using in-cell Western assay. Evaluation of RNA interference for the downregulation of a specific gene in cells by small interfering RNA was performed. Measurements of cytosolic calcium were carried out using the fluorescent dye fura2. Results: Expression of TRPC3 was significantly increased in monocytes from spontaneously hypertensive rats (SHR) compared with normotensive Wistar-Kyoto rats (WKY). Transplasmamembrane calcium influx and thapsigargin-induced sustained calcium increase were significantly higher in SHR compared with WKY. In the presence of the TRP channel blocker SKF-96365 these differences were no longer observed. Specific TRPC3-knockdown by transfection of monocytes from SHR with small interfering RNA significantly reduced TRPC3 expression, trans-plasma membrane calcium influx, and thapsigargin-induced sustained calcium increase. Conclusions: This study shows, for the first time, increased TRPC3 channel expression and increased TRPC3-related calcium influx in SHR. Am J Hypertens 2005;18:1503-1507 (c) 2005 American Journal of Hypertension, Ltd.
引用
收藏
页码:1503 / 1507
页数:5
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