van Breemen C, Chen Q, Laher I
Department of Pharmacology & Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, Canada.
Trends Pharmacol Sci. 1995 Mar;16(3):98-105. doi: 10.1016/s0165-6147(00)88990-7.
In smooth muscle the superficial sarcoplasmic reticulum accumulates a portion of the Ca2+ that enters cells through the plasmalemma and thus functions as a buffer barrier to Ca2+ entry into the myoplasm (superficial buffer barrier or SBB). In this review Cornelis van Breemen, Qian Chen and Ismail Laher summarize experimental support for the SBB, and discuss data indicating that: (1) contraction is related more to the rate than extent of Ca2+ entry; (2) refilling of sarcoplasmic reticulum from the extracellular space is mediated by Ca2+ influx and Ca2+ pumping by the sarcoplasmic reticulum Ca2+ pump; (3) the superficial sarcoplasmic reticulum unloads Ca2+ to the extracellular space by a multi step process that involves sequentially the opening of Ca2+ and inositol 1,4,5-trisphosphate [Ins(1,4,5,)P3] sensitive channels and Ca2+ extrusion by Na(+)-Ca2+ exchange; (4) the SBB generates a peripheral Ca2+ gradient; (5) Ca(2+)-mobilizing receptor agonists generate Ins(1,4,5)P3 which short circuits the SBB to increase the effectiveness of Ca2+ influx in raising [Ca2+]i and consequently increase smooth muscle contraction. A physiologically regulated SBB is thought to enhance the informational content of Ca2+ signalling and support variable reduction of smooth muscle tone. Pharmacological modulation of Ca2+ transport in the superficial sarcoplasmic reticulum therefore presents an alternative means of controlling smooth muscle tone dependent on Ca2+ entry.
在平滑肌中，表层肌浆网会积累一部分通过质膜进入细胞的Ca2+，因此起到了阻止Ca2+进入肌浆的缓冲屏障作用（表层缓冲屏障或SBB）。在这篇综述中，科内利斯·范·布雷门、陈谦（音译）和伊斯梅尔·拉希尔总结了支持SBB的实验证据，并讨论了以下数据：（1）收缩与Ca2+进入的速率而非程度更相关；（2）肌浆网从细胞外空间的再填充是由Ca2+内流和肌浆网Ca2+泵的Ca2+泵浦介导的；（3）表层肌浆网通过一个多步骤过程将Ca2+卸载到细胞外空间，该过程依次涉及Ca2+和肌醇1,4,5-三磷酸[Ins(1,4,5)P3]敏感通道的开放以及通过Na(+)-Ca2+交换进行的Ca2+外排；（4）SBB产生外周Ca2+梯度；（5）Ca(2+)动员受体激动剂产生Ins(1,4,5)P3，它使SBB短路，以提高Ca2+内流在升高[Ca2+]i方面的有效性，从而增加平滑肌收缩。一种生理调节的SBB被认为可以增强Ca2+信号的信息含量，并支持平滑肌张力的可变降低。因此，对表层肌浆网中Ca2+转运的药理学调节提供了一种依赖于Ca2+进入来控制平滑肌张力的替代方法。
