Désilets M, Driska S P, Baumgarten C M
Department of Physiology, University of Ottawa, Ontario, Canada.
Circ Res. 1989 Sep;65(3):708-22. doi: 10.1161/01.res.65.3.708.
Electrical activity of enzymatically isolated, smooth muscle cells from hog carotid arteries was recorded under current clamp and voltage clamp. Under the experimental conditions, membrane potential usually was not stable, and spontaneous hyperpolarizing transients of approximately 100-msec duration were recorded. The amplitude of the transients was markedly voltage dependent and ranged from about 20 mV at a membrane potential of 0 mV to undetectable at membrane potentials negative to -60 mV. Under voltage clamp, transient outward currents displayed a similar voltage dependency. These fluctuations reflect a K+ current; they were abolished by 10 mM tetraethylammonium chloride, a K+ channel blocker, and the current fluctuations reversed direction in high extracellular K+ concentration. Modulators of intracellular Ca2+ concentration also affected electrical activity. Lowering intracellular Ca2+ concentration by addition of 10 mM EGTA to the pipette solution or suppressing sarcoplasmic reticulum function by superfusion with caffeine (10 mM), ryanodine (1 microM), or histamine (3-10 microM) blocked the rapid voltage and current spikes. However, caffeine and histamine induced a much slower hump of outward current before blocking the rapid spikes. This slower transient outward current could be elicited only once after external Ca2+ was removed and is consistent with an activation of K+ channels by Ca2+ released from internal stores. In contrast, removal of external Ca2+ alone failed to abolish the rapid spikes. These results suggest that 1) a Ca2+-dependent K+ conductance can markedly affect the electrical behavior of arterial smooth muscle cells and 2) internal Ca2+ stores, probably the sarcoplasmic reticulum, can support rapid and frequent releases of Ca2+. Exposure to a low concentration of histamine (3 microM) caused synchronization of the irregular, rapid fluctuations giving rise to slow, periodic oscillations of Ca2+-activated K+ conductance with a frequency of 0.1-0.3 Hz. These regular oscillations are reminiscent of periodic Ca2+-induced Ca2+ release, were inhibited by 10 mM caffeine, and point to a modulation of sarcoplasmic reticulum Ca2+ release by histamine.
在电流钳和电压钳条件下，记录了从猪颈动脉酶解分离得到的平滑肌细胞的电活动。在实验条件下，膜电位通常不稳定，记录到了持续时间约100毫秒的自发性超极化瞬变。这些瞬变的幅度明显依赖于电压，范围从膜电位为0 mV时的约20 mV到膜电位为 -60 mV时无法检测到。在电压钳条件下，瞬态外向电流表现出类似的电压依赖性。这些波动反映了一种钾电流；它们被10 mM四乙铵氯（一种钾通道阻滞剂）消除，并且在高细胞外钾浓度下电流波动方向反转。细胞内钙离子浓度的调节剂也影响电活动。通过向移液管溶液中添加10 mM乙二醇双四乙酸（EGTA）降低细胞内钙离子浓度，或通过用咖啡因（10 mM）、ryanodine（1 microM）或组胺（3 - 10 microM）灌注抑制肌浆网功能，可阻断快速的电压和电流尖峰。然而，咖啡因和组胺在阻断快速尖峰之前诱导出一个慢得多的外向电流驼峰。这种较慢的瞬态外向电流在去除细胞外钙离子后只能诱发一次，并且与从内部储存释放的钙离子激活钾通道一致。相比之下，仅去除细胞外钙离子未能消除快速尖峰。这些结果表明：1）一种钙依赖性钾电导可显著影响动脉平滑肌细胞的电行为；2）细胞内钙储存，可能是肌浆网，可支持钙离子的快速和频繁释放。暴露于低浓度组胺（3 microM）会使不规则的快速波动同步，导致钙激活钾电导的缓慢、周期性振荡，频率为0.1 - 0.3 Hz。这些规则振荡让人联想到周期性的钙诱导钙释放，被10 mM咖啡因抑制，并表明组胺对肌浆网钙释放有调节作用。
