Lack of nitric oxide synthase depresses ion transporting enzyme function in cardiac muscle.
Lack of nitric oxide synthase depresses ion transporting enzyme function in cardiac muscle.
复制标题
一氧化氮合酶的缺乏会抑制心肌中离子转运酶的功能。
DOI：
10.1016/s0006-291x(02)00599-5
复制
发表时间：
2002
影响因子：
3.1
通讯作者：
Xu,KaiY
中科院分区：
文献类型：
--
作者：
Zhou,Lan;Burnett,ArthurL;Huang,PaulL;Becker,LewisC;Kuppusamy,Periannan;Kass,DavidA;KevinDonahue,J;Proud,David;Sham,JamesSK;Dawson,TedM;Xu,KaiY
Nitric oxide (NO) is produced endogenously from NOS isoforms bound to sarcolemmal (SL) and sarcoplasmic reticulum (SR) membranes. To investigate whether locally generated NO directly affects the activity of enzymes mediating ion active transport, we studied whether knockout of selected NOS isoforms would affect the functions of cardiac SL (Na++K+)-ATPase and SR Ca2+-ATPase. Cardiac SL and SR vesicles containing either SL (Na++K+)-ATPase or SR Ca2+-ATPase were isolated from mice lacking either nNOS or eNOS, or both, and tested for enzyme activities. Western blot analysis revealed that absence of single or double NOS isoforms did not interrupt the protein expression of SL (Na++K+)-ATPase and SR Ca2+-ATPase in cardiac muscle cells. However, lack of NOS isoforms in cardiac muscle significantly altered both (Na++K+)-ATPase activity and SR Ca2+-ATPase function. Our experimental results suggest that disrupted endogenous NO production may change local redox conditions and lead to an unbalanced free radical homeostasis in cardiac muscle cells which, in turn, may affect key enzyme activities and membrane ion active transport systems in the heart.
