前列腺素可激活大鼠主动脉中的磷酸肌醇代谢。

Prostaglandins activate phosphoinositide metabolism in rat aorta.

作者信息

Suba E A, Roth B L

出版信息

Eur J Pharmacol. 1987 Apr 29;136(3):325-32. doi: 10.1016/0014-2999(87)90305-0.

Abstract

The ability of the five prostaglandins to activate phosphoinositide (PI) metabolism and to induce contraction was studied in rat aorta. All prostaglandins (PG) tested (B2, D2, E2, F1 alpha and F2 alpha) stimulated PI hydrolysis in the range of 0.01-1,000 microM (EC50 s from 0.9 to 47 microM) and elicited contractions in the range of 0.1-100 microM (EC50 s from 0.3 to 22.1 microM). The rank order potency was PGD2 greater than F2 alpha greater than F1 alpha greater than E2 greater than B2 for PI hydrolysis and PGB2 greater than F2 alpha greater than D2 greater than E2 greater than F1 alpha for contraction. The activation of PI hydrolysis by the various prostaglandins was greater than or equal to the effect of 5-hydroxytryptamine, norepinephrine, angiotensin II and [Arg8]vasopressin. The PI hydrolytic activity of PGD2, E2 and F2 alpha correlated with their ability to induce contraction. The results with PGB2 and F1 alpha showed, however, that activation of PI hydrolysis per se is not always a sufficient or necessary condition for rat aortic contraction.

摘要

在大鼠主动脉中研究了五种前列腺素激活磷酸肌醇（PI）代谢和诱导收缩的能力。所有测试的前列腺素（PG）（B2、D2、E2、F1α和F2α）在0.01 - 1000微摩尔范围内刺激PI水解（EC50为0.9至47微摩尔），并在0.1 - 100微摩尔范围内引发收缩（EC50为0.3至22.1微摩尔）。对于PI水解，效力顺序为PGD2＞F2α＞F1α＞E2＞B2；对于收缩，效力顺序为PGB2＞F2α＞D2＞E2＞F1α。各种前列腺素对PI水解活性的激活作用大于或等于5-羟色胺、去甲肾上腺素、血管紧张素II和[Arg8]加压素的作用。PGD2、E2和F2α的PI水解活性与其诱导收缩的能力相关。然而，PGB2和F1α的结果表明，就大鼠主动脉收缩而言，PI水解的激活本身并不总是一个充分或必要条件。