[血管活性肠肽（VIP）诱导的、由内皮舒张因子/一氧化氮（EDRF/NO）介导的离体灌注大鼠肺血管舒张]

[Vasoactive intestinal peptide (VIP)-induced pulmonary vasodilation mediated by EDRF/NO in isolated perfused rat lungs].

作者信息

Iwabuchi S, Ono S, Funata J, Hoshikawa Y, Ueda S, Ashino Y, Tanita T, Fujimura S, Koike K

机构信息

Department of Thoracic Surgery, Tohoku University, Sendai, Japan.

出版信息

Nihon Kyobu Shikkan Gakkai Zasshi. 1995 Mar;33(3):262-7.

PMID:7739167

Abstract

We studied the effects of Vasoactive Intestinal Peptide (VIP) on the pulmonary circulation in isolated perfused rat lungs. VIP caused pulmonary vasodilation in a dose-dependent manner. This effect was inhibited by pretreatment with L-N omega-nitro-arginine (L-NNA), a competitive inhibitor of endothelium-derived relaxing factor (EDRF/NO), but not by meclofenamate, a cyclooxygenase inhibitor. Addition of L-arginine, a substrate of EDRF/NO, after treatment with L-NNA reversed VIP-induced pulmonary vasodilation. These results indicate that VIP causes pulmonary vasodilation, and they suggest a role for EDRF/NO in VIP-induced pulmonary vasodilation in isolated rat lungs.

摘要

我们研究了血管活性肠肽（VIP）对离体灌流大鼠肺脏肺循环的影响。VIP 以剂量依赖的方式引起肺血管舒张。这种效应可被内皮源性舒张因子（EDRF/NO）的竞争性抑制剂 L-Nω-硝基精氨酸（L-NNA）预处理所抑制，但不能被环氧化酶抑制剂甲氯芬那酸所抑制。在用 L-NNA 处理后添加 EDRF/NO 的底物 L-精氨酸可逆转 VIP 诱导的肺血管舒张。这些结果表明 VIP 可引起肺血管舒张，并提示 EDRF/NO 在离体大鼠肺脏中 VIP 诱导的肺血管舒张中发挥作用。