Van Renterghem C, Vigne P, Barhanin J, Schmid-Alliana A, Frelin C, Lazdunski M
Centre de Biochimie du Centre National de la Recherche Scientifique, Nice, France.
Biochem Biophys Res Commun. 1988 Dec 30;157(3):977-85. doi: 10.1016/s0006-291x(88)80970-7.
Endothelin, one of the most potent vasoconstrictor known, has been suggested to act as an endogenous agonist of L-type Ca2+ channels. In this paper we show that endothelin stimulates the metabolism of inositol phosphates and induces the mobilization of intracellular Ca2+ stores. The transient activation of Ca2+-sensitive K+ channel provokes an hyperpolarization of the membrane. It is followed by a sustained depolarization which is due to the opening of a non-specific cation channel which is permeable to Ca2+ and Mg2+. The depolarization then activates L-type Ca2+ channels. This mechanism of action explains why part of the endothelin-induced vasocontriction is eliminated by L-type Ca2+ channel blockers.
内皮素是已知最强效的血管收缩剂之一，有人提出它可作为L型钙通道的内源性激动剂。在本文中，我们表明内皮素可刺激肌醇磷酸的代谢并诱导细胞内钙库的动员。钙敏钾通道的瞬时激活引发膜的超极化。随后是持续的去极化，这是由于一个对Ca2+和Mg2+通透的非特异性阳离子通道开放所致。然后去极化激活L型钙通道。这种作用机制解释了为什么L型钙通道阻滞剂可消除部分内皮素诱导的血管收缩。
