Na+ and modulation of Na+/Ca2+ exchange as a key mechanism of TRPC signaling

被引：48

作者：

Eder, P

Poteser, M

Romanin, C

Groschner, K

机构：

[1] Karl Franzens Univ Graz, Inst Pharmaceut Sci, A-8010 Graz, Austria

[2] Univ Linz, Inst Biophys, A-4020 Linz, Austria

来源：

PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY | 2005年 / 451卷 / 01期

关键词：

TRPC proteins; non-selective cation channels; Ca2+ signaling; Na+/Ca2+ exchange;

D O I：

10.1007/s00424-005-1434-2

中图分类号：

Q4 [生理学];

学科分类号：

071003 ;

摘要：

Ion channels formed by canonical transient receptor potential ( TRPC) proteins are considered to be key players in cellular Ca2+ homeostasis. As permeation of Ca2+ through TRPC homo- and/or heteromeric channels has been repeatedly demonstrated, analysis of the physiological role of TRPC proteins was so far based on the concept that these proteins form regulated Ca2+ entry channels. The well-recognized lack of cation selectivity of TRPC channels and the ability to generate substantial monovalent conductances that govern membrane potential and cation gradients were barely appreciated as a physiologically relevant issue. Nonetheless, recent studies suggest monovalent, specifically Na+ permeation through TRPC cation channels as an important event in TRPC signaling. TRPC-mediated Na+ entry may be converted into a distinct pattern of cellular Ca2+ signals by interaction with Na+/ Ca2+ exchanger proteins. This review discusses current concepts regarding the link between Na+ entry through TRPC channels and cellular Ca2+ signaling.

引用

页码：99 / 104

页数：6

共 30 条

[21] Crosstalk between voltage-independent Ca2+ channels and L-type Ca2+ channels in A7r5 vascular smooth muscle cells at elevated intracellular pH -: Evidence for functional coupling between L-type Ca2+ channels and a 2-APB-sensitive cation channel [J].