血管紧张素可诱导兔输精管释放前列环素：受体异质性的证据。

Angiotensins induce the release of prostacyclin from rabbit vas deferens: evidence for receptor heterogeneity.

作者信息

Catalioto R M, Renzetti A R, Criscuoli M, Mizrahi J, Subissi A

机构信息

Department of Pharmacology, Laboratori Guidotti S.p.A., Pisa, Italy.

出版信息

Eur J Pharmacol. 1994 Apr 11;256(1):93-7. doi: 10.1016/0014-2999(94)90621-1.

DOI:10.1016/0014-2999(94)90621-1

PMID:8026565

Abstract

Angiotensin II and angiotensin III stimulated prostacyclin release in a time- and dose-dependent manner in both the prostatic and the non-prostatic part of the rabbit vas deferens. Also, angiotensin I enhanced the production of prostacyclin and its effect was blocked by captopril. Losartan, a type 1 (angiotensin AT1)-selective receptor antagonist, prevented the angiotensin II-induced prostacyclin release. The agonist peptide, p-aminophenylalanine angiotensin II, and the type 2 (angiotensin AT2)-selective receptor antagonist, PD123319, were found active only in the prostatic portion, suggesting heterogeneity of the receptor population. In conclusion, an angiotensin AT1 receptor mostly mediates the angiotensin-induced release of prostacyclin in the rabbit vas deferens.

摘要

血管紧张素II和血管紧张素III以时间和剂量依赖性方式刺激兔输精管前列腺部和非前列腺部的前列环素释放。此外，血管紧张素I增强了前列环素的生成，其作用被卡托普利阻断。1型（血管紧张素AT1）选择性受体拮抗剂氯沙坦可阻止血管紧张素II诱导的前列环素释放。激动剂肽对氨基苯丙氨酸血管紧张素II和2型（血管紧张素AT2）选择性受体拮抗剂PD123319仅在前列腺部有活性，提示受体群体存在异质性。总之，血管紧张素AT1受体主要介导血管紧张素诱导的兔输精管前列环素释放。