血管加压素通过V1受体抑制人血小板微粒体部分的腺苷酸环化酶活性。

Vasopressin inhibits the adenylate cyclase activity of human platelet particulate fraction through V1-receptors.

作者信息

Vanderwel M, Lum D S, Haslam R J

出版信息

FEBS Lett. 1983 Dec 12;164(2):340-4. doi: 10.1016/0014-5793(83)80313-5.

Abstract

Arg8-vasopressin inhibited the adenylate cyclase activity of human platelet particulate fraction up to a maximum of 27% (IC50 = 1.2 nM). This inhibition required the presence of 10 microM GTP and was optimal with 100 mM NaCl. Orn8-vasopressin had similar effects. 1-Deamino-Val4, D-Arg8-vasopressin did not by itself affect adenylate cyclase activity but competitively inhibited the action of Arg8-vasopressin (pA2 = 7.74). Arg8-vasopressin did not inhibit adenylate cyclase in intact platelets but instead caused platelet aggregation, an effect that was also competitively inhibited by 1-deamino-Val4, D-Arg8-vasopressin (pA2 = 7.82). Thus, platelets possess vasopressin receptors of the V1 type that, under appropriate conditions, can mediate either inhibition of platelet adenylate cyclase or platelet aggregation.

摘要

精氨酸8 - 加压素对人血小板微粒体部分的腺苷酸环化酶活性的抑制作用最高可达27%（半数抑制浓度IC50 = 1.2 nM）。这种抑制作用需要10 μM鸟苷三磷酸（GTP）的存在，在100 mM氯化钠时效果最佳。鸟氨酸8 - 加压素具有类似的作用。1 - 脱氨基 - 缬氨酸4，D - 精氨酸8 - 加压素本身并不影响腺苷酸环化酶活性，但能竞争性抑制精氨酸8 - 加压素的作用（拮抗常数pA2 = 7.74）。精氨酸8 - 加压素在完整血小板中并不抑制腺苷酸环化酶，反而引起血小板聚集，这一效应也受到1 - 脱氨基 - 缬氨酸4，D - 精氨酸8 - 加压素的竞争性抑制（pA2 = 7.82）。因此，血小板具有V1型加压素受体，在适当条件下，该受体可介导血小板腺苷酸环化酶的抑制或血小板聚集。