P1,P4-二腺苷5′-四磷酸诱导牛主动脉内皮细胞释放一氧化氮。

P1,P4-diadenosine 5' tetraphosphate induces nitric oxide release from bovine aortic endothelial cells.

作者信息

Hilderman R H, Christensen E F

机构信息

Department of Microbiology/Molecular Medicine, Greenville Hospital System/Clemson University Biomedical Cooperative, SC 29634-1903, USA.

出版信息

FEBS Lett. 1998 May 15;427(3):320-4. doi: 10.1016/s0014-5793(98)00454-2.

DOI:10.1016/s0014-5793(98)00454-2

PMID:9637249

Abstract

Since the infusion of P1,P4-diadenosine 5' tetraphosphate (Ap4A) into animal models induces vasodilation [1,2], the present study was performed to determine whether Ap4A induces the release of nitric oxide (NO) from endothelial cells. Ap4A induced NO release was 4.2-fold greater than the amount of NO released under basal condition. Ap4A induced NO release was inhibited by NG-nitro-L-arginine (L-NNA) and this inhibition was reversed by L-Arg. In addition, EGTA inhibits Ap4A induced NO release. These data are consistent with Ap4A inducing the release of NO from endothelial cells through the activation of endothelial nitric oxide synthase.

摘要

由于将P1，P4 - 二腺苷5'-四磷酸（Ap4A）注入动物模型会引起血管舒张[1,2]，因此进行本研究以确定Ap4A是否会诱导内皮细胞释放一氧化氮（NO）。Ap4A诱导的NO释放比基础条件下释放的NO量高4.2倍。Ap4A诱导的NO释放受到NG-硝基-L-精氨酸（L-NNA）的抑制，并且这种抑制作用可被L-精氨酸逆转。此外，乙二醇双（2-氨基乙基醚）四乙酸（EGTA）抑制Ap4A诱导的NO释放。这些数据与Ap4A通过激活内皮型一氧化氮合酶诱导内皮细胞释放NO一致。