INTRACELLULAR ALUMINUM INHIBITS ACETYLCHOLINE-EVOKED AND CAFFEINE-EVOKED CA2+ MOBILIZATION

被引：26

作者：

WAKUI, M ^{[1
]}

ITAYA, K ^{[1
]}

BIRCHALL, D ^{[1
]}

PETERSEN, OH ^{[1
]}

机构：

[1] UNIV LIVERPOOL,PHYSIOL LAB,CNRS,SECRETORY CONTROL RES GRP,POB 147,LIVERPOOL L69 3BX,ENGLAND

来源：

FEBS LETTERS | 1990年 / 267卷 / 02期

关键词：

Acetylcholine; Aluminium; Ca[!sup]2+[!/sup]-activated Cl[!sup]-[!/sup] current; Caffeine;

D O I：

10.1016/0014-5793(90)80949-J

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The effect of in tracellular aluminium on Ca2+ signalling in single internally perfused mouse pancreatic acinar cells was investigated by measurement of the Ca2+-dependent Cl- current using the patch-clamp whole-cell recording configuration. Acetylcholine (ACh) normally evoked a pulsatile Ca2+-dependent Cl- current, but when A1C13 (1 mM) was present in the internal perfusion solution the ACh responses were virtually absent. When aluminium was acutely infused into the internal perfusion solution, the ACh-evoked Ca2+ signals and also the caffeine-evoked responses quickly disappeared, but the Ca2+ ionophore, ionomycin (100 nM), could still induce a large increase in the Cl- current. It is concluded that intracellular aluminium can abolish receptor-activated intracellular Ca2+ release probably by inhibition of Ca2+-induced Ca2+ release. © 1990.

引用

页码：301 / 304

页数：4

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