Endothelial release of tissue-type plasminogen activator in the human forearm: role of nitric oxide.
Endothelial release of tissue-type plasminogen activator in the human forearm: role of nitric oxide.
复制标题
人前臂组织型纤溶酶原激活剂的内皮释放：一氧化氮的作用。
DOI：
10.1097/00005344-200308000-00022
复制
发表时间：
2003
影响因子：
3
通讯作者：
DeSouza,ChristopherA
中科院分区：
文献类型：
--
作者：
Smith,DerekT;Hoetzer,GretaL;Greiner,JaredJ;Stauffer,BrianL;DeSouza,ChristopherA
Release of tissue-type plasminogen activator (t-PA) from the vascular endothelium is paramount to endogenous thrombolysis potential. In addition to its vasodilator effects, nitric oxide (NO) has important antithrombotic properties, such as inhibition of platelet aggregation. It is currently not clear whether NO influences the capacity of the endothelium to release t-PA. The authors determined whether net endothelial t-PA release is regulated, at least in part, by NO. Endothelial t-PA release was determined, in vivo, in response to intrabrachial infusions of bradykinin (12.5–50.0 ng· 100 mL tissue− 1· min− 1) in the presence and absence of the NO synthase inhibitor, N G-monomethyl-l-arginine (l-NMMA; 5 mg/min) in 12 healthy men. Net release of t-PA across the forearm vascular bed was calculated as the product of arteriovenous concentration gradient and forearm plasma flow. The vasodilator response to bradykinin was significantly blunted (∼ 30%) with l-NMMA. Although there was no effect of l-NMMA on basal t-PA release, acute release of t-PA to bradykinin was higher (P< 0.01) after (from–0.2±0.5 to 105.2±9.4 ng· 100 mL tissue− 1· min− 1) versus before (from–0.4±0.7 to 48.7±7.3 ng· 100 mL tissue− 1· min− 1) the administration of l-NMMA. Thus, in the absence of NO endothelial t-PA release was enhanced. These results suggest a potential regulatory influence of NO on bradykinin induced endothelial t-PA release.
