内皮素-1对主动脉细胞作用的分子机制。
Molecular mechanism of endothelin-1 action on aortic cells.
作者信息
Van Renterghem C, Vigne P, Barhanin J, Schmid-Alliana A, Frelin C, Lazdunski M
机构信息
Centre de Biochimie du Centre National de la Recherche Scientifique, Nice, France.
出版信息
J Cardiovasc Pharmacol. 1989;13 Suppl 5:S186-7. doi: 10.1097/00005344-198900135-00051.
The vasoconstricting action of endothelin-1 (ET-1) is partly mediated by voltage-dependent L-type Ca2+ channels. Activation of the Ca2+ channels is indirect. ET-1 action involves (i) the hydrolysis of phosphatidylinositol and the release of Ca2+ from internal stores and (ii) the opening of a nonselective cation channel in the plasma membrane. The resulting depolarization triggers the activity of L-type Ca2+ channels.
内皮素-1（ET-1）的血管收缩作用部分由电压依赖性L型Ca2+通道介导。Ca2+通道的激活是间接的。ET-1的作用涉及：（i）磷脂酰肌醇的水解和细胞内储存的Ca2+释放；（ii）质膜中非选择性阳离子通道的开放。由此产生的去极化触发L型Ca2+通道的活性。
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