内皮素与钙离子激动剂Bay K 8644：不同的血管收缩特性。

Endothelin and Ca++ agonist Bay K 8644: different vasoconstrictive properties.

作者信息

Auguet M, Delaflotte S, Chabrier P E, Pirotzky E, Clostre F, Braquet P

机构信息

Institut Henri Beaufour, Les Ulis, France.

出版信息

Biochem Biophys Res Commun. 1988 Oct 14;156(1):186-92. doi: 10.1016/s0006-291x(88)80822-2.

DOI:10.1016/s0006-291x(88)80822-2

PMID:2460098

Abstract

The mechanism of vasoconstriction induced by endothelin was investigated in rat isolated aorta in comparison with the Ca++ agonist, Bay K 8644. Endothelin (EC50 = 4 nM) induced a slow and sustained contraction in control medium whereas the one elicited by Bay K 8644 (EC50 = 14 nM) necessitating a partly K+ depolarized medium was fast with superimposed rhythmic contraction. By opposition with Bay K 8644, endothelin contraction was not inhibited by the calcium antagonists (1 microM), nifedipine, diltiazem and D 600, and substantially persisted in Ca++ free medium or after depletion of intracellular Ca++ by phenylephrine (1 microM). These data show that endothelin does not act as an activator of potential dependent Ca++ channels but probably through specific receptor(s) as suggested by its mode of vasoconstriction.

摘要

在内皮素诱导血管收缩的机制研究中，以大鼠离体主动脉为研究对象，并与钙离子激动剂Bay K 8644进行对比。内皮素（半数有效浓度EC50 = 4 nM）在对照培养基中诱导出缓慢且持续的收缩，而Bay K 8644（EC50 = 14 nM）诱导的收缩需要部分钾离子去极化培养基，其收缩迅速并伴有叠加的节律性收缩。与Bay K 8644不同，内皮素诱导的收缩不受钙拮抗剂（1 microM）硝苯地平、地尔硫卓和D 600的抑制，并且在无钙培养基中或用去氧肾上腺素（1 microM）耗尽细胞内钙离子后仍基本持续存在。这些数据表明，内皮素并非作为电压依赖性钙离子通道的激活剂起作用，而是可能通过特定受体起作用，这由其血管收缩模式所提示。