Spontaneous transient outward currents in smooth muscle cells

被引:125
作者
Bolton, TB [1 ]
Imaizumi, Y [1 ]
机构
[1] NAGOYA CITY UNIV, DEPT CHEM PHARMACOL, NAGOYA, AICHI, JAPAN
关键词
D O I
10.1016/S0143-4160(96)90103-7
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Spontaneous transient outward currents (STOCs) lasting about 100 ms occur in single smooth muscle cells and represent the simultaneous opening of up to a hundred calcium-activated potassium (BK) channels. The recent observation of brief focal releases of sarcoplasmic reticulum (SR) calcium ('sparks') in smooth muscle cells has provided support for the original suggestion that STOCs arise due to the spontaneous releases of calcium from the SR close to the sarcolemma. However, it is possible that such releases occur in a region of close apposition of SR membrane and sarcolemma about 0.1 mu m wide ('junctional space') in which case they would be detectable by endogenous calcium-sensitive molecules such as BK channels but, using present confocal microscopy technique, not by calcium-indicator dyes introduced into the cell; should calcium escape from the junctional space then it may be visualised as 'sparks' by the fluorescent emission from calcium-indicator dyes using confocal microscopy. Some STOCs seem too large to represent the effect of a single 'spark' and some form of calcium-induced calcium release or 'macrospark' may be involved in their generation. Depletion of calcium stores by caffeine, ryanodine, or by activation of receptors linked to the phospholipase C/inositol trisphosphate system abolishes STOCs. However, low concentrations of caffeine or inositol trisphosphate accelerate STOC discharge by an unknown mechanism and often decrease STOC size presumably by depleting store calcium; similar effects are produced by agents such as cyclopiazonic add and thapsigargin which inhibit calcium storage mechanisms (largely the SR calcium pump).
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页码:141 / 152
页数:12
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