CALCIUM ENTRY THROUGH RECEPTOR-OPERATED CHANNELS IN BOVINE PULMONARY-ARTERY ENDOTHELIAL-CELLS
CALCIUM ENTRY THROUGH RECEPTOR-OPERATED CHANNELS IN BOVINE PULMONARY-ARTERY ENDOTHELIAL-CELLS
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DOI：
10.1016/0040-8166(87)90015-2
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发表时间：
1987-01-01
期刊：
影响因子：
2.6
通讯作者：
ADAMS, DJ
中科院分区：
文献类型：
--
作者：
JOHNS, A;LATEGAN, TW;ADAMS, DJ
应用生物测定法、膜片钳法和~（45）Ca流量法研究了内皮依赖性血管舒张剂对内皮细胞的激活作用。培养的肺动脉内皮细胞已被证明释放EDRF响应凝血酶，缓激肽，ATP和钙离子载体A23187。内皮细胞的静息膜电位为-56mV，增加细胞外K ~+或加入（0.1-1.0mM）Ba ~（2+）使细胞去极化。培养的内皮细胞的电生理特性表明，膜电位是由一个内向整流钾通道维持的，平均单通道电导为36- 6pS。去极化激活的内向电流的情况下，45 Ca内流与高K+溶液的减少表明，没有功能性的电压依赖性钙或钠通道。凝血酶和缓激肽不仅引起内向电流（由Na+和Ca 2+携带），而且还增加了45 Ca内流，这表明EDRF释放所需的细胞内钙的增加是由受体操作通道的开放介导的。高剂量的凝血酶和缓激肽可引起细胞内钙释放，而低剂量的凝血酶则不能引起细胞内钙释放。我们提出，内皮依赖性血管扩张剂诱导的内皮细胞胞浆钙浓度增加是由于Ca 2+通过受体操作的离子通道流入，并在较小程度上从尚未定义的细胞内储存的钙释放。
The activation of endothelial cells by endothelium-dependent vasodilators has been investigated using bioassay, patch clamp and 45Ca flux methods. Cultured pulmonary artery endothelial cells have been demonstrated to release EDRF in response to thrombin, bradykinin, ATP and the calcium ionophore A23187. The resting membrane potential of the endothelial cells was -56 mV and the cells were depolarized by increasing extracellular K+ or by the addition of (0.1-1.0mM) Ba2+ to the bathing solution. The electrophysiological properties of the cultured endothelial cells suggest that the membrane potential is maintained by an inward rectifying K+ channel with a mean single channel conductance of 36-6 pS. The absence of a depolarization activated inward current and the reduction of 45Ca influx with high K+ solution suggests that there are no functional voltage-dependent calcium or sodium channels. Thrombin and bradykinin were shown to evoke not only an inward current (carried by Na+ and Ca2+) but also an increase in 45Ca influx suggesting that the increase in intracellular calcium necessary for EDRF release is mediated by an opening of a receptor operated channel. High doses of thrombin and bradykinin induced intracellular calciumrelease, however, at low doses of thrombin no intracellular calcium release was observed. We propose that the increased cytosolic calcium concentration in endothelial cells induced by endothelium dependent vasodilators is due to the influx of Ca2+ through a receptor operated ion channel and to a lesser degree to intracellular release of calcium from a yet undefined intracellular store.