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
突变体
酶
血压
药理学
生物化学
内科学
医学
基因
半胱氨酸
有机化学
硫黄
作者
Guangdong Yang,Zhenhua Wu,Bo Jiang,Wei Yang,Jiansong Qi,Kun Cao,Qinghe Meng,Asif K. Mustafa,Weitong Mu,Shengming Zhang,Solomon H. Snyder,Rui Wang
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2008-10-23
卷期号:322 (5901): 587-590
被引量:2177
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 (H 2 S) is now receiving increasing attention. Here we show that H 2 S is physiologically generated by cystathionine γ-lyase (CSE) and that genetic deletion of this enzyme in mice markedly reduces H 2 S 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 H 2 S formation in response to vascular activation. These findings provide direct evidence that H 2 S is a physiologic vasodilator and regulator of blood pressure.
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