前列腺素和激肽对血管加压素刺激的水流动的独立作用。

Independent action of prostaglandins and kinins on vasopressin-stimulated water flow.

作者信息

Carvounis G, Carvounis C P, Arbeit L A

出版信息

Kidney Int. 1985 Mar;27(3):512-6. doi: 10.1038/ki.1985.40.

DOI:10.1038/ki.1985.40

Abstract

The kallikrein-kinin and the prostaglandin systems are both important modifiers of vasopressin action. This study examines whether the systems are dependent on one another for their action. Four groups of toad hemibladders were examined. In groups 1 and 2 animals the endogenous prostaglandin system was inhibited. Inhibition of kallikrein by aprotinin caused vasopressin-stimulated water flow to increase further (24.8 +/- 4.9 to 34.5 +/- 4.8 microliters/min) while potentiation of kinins by captropril caused vasopressin-stimulated water flow to decrease (45 +/- 6.3 to 30.5 +/- 5.4 microliters/min). In groups 3 and 4 endogenous kallikrein was inhibited by aprotinin. The addition of prostaglandin E2 caused vasopressin-stimulated water flow to decrease (17.5 +/- 2.7 to 5.71 +/- 1.0 microliter/min) while the inhibition of endogenous prostaglandins caused vasopressin-stimulated water flow to increase (26.7 +/- 3.4 to 39.2 +/- 3.5 microliters/min). Thus, the inhibitory effects of prostaglandins and kinins on vasopressin-stimulated water flow are independent of one another.

摘要

激肽释放酶 - 激肽系统和前列腺素系统都是血管加压素作用的重要调节因子。本研究探讨了这两个系统的作用是否相互依赖。对四组蟾蜍半膀胱进行了检查。在第1组和第2组动物中，内源性前列腺素系统受到抑制。抑肽酶抑制激肽释放酶导致血管加压素刺激的水流量进一步增加（从24.8±4.9微升/分钟增加到34.5±4.8微升/分钟），而卡托普利增强激肽则导致血管加压素刺激的水流量减少（从45±6.3微升/分钟减少到30.5±5.4微升/分钟）。在第3组和第4组中，抑肽酶抑制内源性激肽释放酶。添加前列腺素E2导致血管加压素刺激的水流量减少（从17.5±2.7微升/分钟减少到5.71±1.0微升/分钟），而抑制内源性前列腺素则导致血管加压素刺激的水流量增加（从26.7±3.4微升/分钟增加到39.2±3.5微升/分钟）。因此，前列腺素和激肽对血管加压素刺激的水流量的抑制作用相互独立。