内源性一氧化氮合酶抑制物与肺动脉高压研究进展  

Research progress of Endogenous inhibitor of nitric oxide synthase in pulmonary hypertension

作　　者：曹仕鹏[1] 诸兰艳[2] 

机构地区：[1]湖南省长沙市中心医院呼吸内科 [2]中南大学湘雅二医院呼吸内科

出　　处：《临床医药实践》2009年第8X期565-568,共4页Proceeding of Clinical Medicine

摘　　要：内源性一氧化氮合酶抑制物非对称二甲基精氨酸(ADMA)是近年来的研究热点,被认为是一种新的心血管疾病风险因子。其代谢主要经二甲基精氨酸二甲胺水解酶(DDAH)水解途径完成。ADMA/DDAH通路的失调可能引起内皮功能不全、肺血管重构等一系列病理改变并导致肺动脉高压形成。阐明ADMA在肺动脉发生发展中的作用对肺动脉高压防治具有重要意义。Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase, which has been con-sidered a new risk factor for cardiovascular disease. Hydrolysis by dimethylarginine dimethylaminehydrolase (DDAH) is the major metabolism way of ADMA. ADMA/DDAH pathway may lead to an imbalance in endothelial dysfunction, pulmonary vascular remodeling, such as a series of pathological changes and lead to the formation of pulmonary hypertension(PH). It will be of great significance to clarify the role of ADMA in the occurrence and development of pulmonary hypertension for a treatment for PH.

关 键 词：ADMA DDAH 肺动脉高压 

分 类 号：R543[医药卫生—心血管疾病]