胱硫醚β合酶
胱硫醚γ裂解酶
一氧化氮
血管舒张
硫化氢
化学
钙
酶
血压
药理学
生物化学
内科学
内分泌学
医学
半胱氨酸
硫黄
有机化学
作者
Guangdong Yang,Lingyun Wu,Shu-Jiang Tu,Wei Yang,Jiansong Qi,Kun Cao,Qinghe Meng,Asif K. Mustafa,Weitong Mu,Shengming Zhang,Solomon H. Snyder,Rong Wang
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2008-10-24
卷期号:322 (5901): 587-590
被引量:2005
标识
DOI:10.1126/science.1162667
摘要
Studies of nitric oxide over the past two decades have highlighted the fundamental importance of gaseous signaling molecules in biology and medicine. The physiological role of other gases such as carbon monoxide and hydrogen sulfide (H2S) is now receiving increasing attention. Here we show that H2S is physiologically generated by cystathionine gamma-lyase (CSE) and that genetic deletion of this enzyme in mice markedly reduces H2S levels in the serum, heart, aorta, and other tissues. Mutant mice lacking CSE display pronounced hypertension and diminished endothelium-dependent vasorelaxation. CSE is physiologically activated by calcium-calmodulin, which is a mechanism for H2S formation in response to vascular activation. These findings provide direct evidence that H2S is a physiologic vasodilator and regulator of blood pressure.
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