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在A7r5血管平滑肌细胞中,三磷酸肌醇(IP3)诱导的钙离子(Ca2+)释放代表着钙库的部分排空,而非独立量子的全或无式钙离子释放。

IP3-induced Ca2+ release in A7r5 vascular smooth-muscle cells represents a partial emptying of the stores and not an all-or-none Ca2+ release of separate quanta.

作者信息

Missiaen L, Sipma H, Parys J B, De Smet P, Callewaert G, Hill E, McCarthy T V, De Smedt H

机构信息

Laboratorium voor Fysiologie, K.U. Leuven Campus Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium.

出版信息

Pflugers Arch. 1999 Apr;437(5):691-4. doi: 10.1007/s004240050833.

Abstract

There is still no agreement on the mechanism of the intracellular action of low concentrations of inositol 1,4,5-trisphosphate (IP3). Intracellular Ca2+ stores may transiently release some Ca2+ before they become insensitive to IP3. Alternatively, stores with a low IP3 threshold may lose all their Ca2+ and the others none. We now report that the IP3 threshold was not correlated with the extent of Ca2+ release in permeabilized A7r5 smooth-muscle cells. In contrast, the maximum rate of release, which was changed either by varying the level of IP3 receptor (IP3R) activation, or by changing the concentration of IP3R at a constant level of IP3R activation, was directly related to the extent of Ca2+ release. We conclude that IP3-induced Ca2+ release reflects partial emptying of the stores and not all-or-none Ca2+ release of separate quanta.

摘要

关于低浓度肌醇1,4,5 -三磷酸(IP3)的细胞内作用机制,目前仍未达成共识。细胞内钙库在对IP3变得不敏感之前,可能会短暂释放一些Ca2+。或者,IP3阈值低的钙库可能会释放其所有的Ca2+,而其他的则不会。我们现在报告,在通透的A7r5平滑肌细胞中,IP3阈值与Ca2+释放程度无关。相反,通过改变IP3受体(IP3R)激活水平或在IP3R激活水平恒定的情况下改变IP3R浓度而改变的最大释放速率,与Ca2+释放程度直接相关。我们得出结论,IP3诱导的Ca2+释放反映了钙库的部分排空,而不是单个量子的全或无Ca2+释放。

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