一氧化氮、一氧化氮合酶和心脏功能

一氧化氮合酶(nitric　oxide synthase,NOS)催化L-精氨酸的氧化反应生成L-胍氨酸和一氧化氮(nitric oxide,NO)。其产物NO可通过依赖cGMP(环磷酸鸟苷)途径与非依赖cGMP途径发挥其复杂的生理学功能,如在心血管系统具有维持血管张力、调节血压,抑制血管平滑肌细胞迁移、增生,抑制血小板聚集与白细胞对血管壁的粘附以及调节影响心肌收缩与舒张功能的作用,并参与心率变异调节功能。本文就3种NOS同工酶的基因及其基因表达调节及影响因素进行简要综述。着重介绍nNOS1的心脏自主神经调节机制,iNOS对心脏收缩抑制以及心脏保护与损伤的双重作用,并对eNOS参与心功能调节的机制及其它生理、病理学等方面研究进展进行综述。

Nitric Oxide,Nitric Oxide Synthase and Cardiac Function

Nitric oxide synthases( NOSs) catalyze the conversion of the cationic amino acid L-arginine to L-citrul-line and nitric oxide (NO ). NO plays its complex biological roles by a dependent cycle guanine nucleotide mono-phosphate (cGMP) pathway and an independent cGMP pathway, such as maintaining vascular tone , regulating bloodpressure ,inhibiting vascular smooth muscle cell migration and proliferation ,inhibiting platelet aggregation and leuko-cyte adhesion to vascular wall, and regulating myocardial contraction and diastolic function, .and so on. NO also playsroles in the regulation of heart rate variability. We focused on the gene structure , regulation of gene expression andthier influence factors in three isoforms of NOS. We intensively introduced the role of neuronal NOS (nNOS) incardiac autonomous nerve regulation and the dual roles of inducible NOS( iNOS) in inhibiting cardiac contraction andcarrying heart protection and damage, and then reviewed the study progresses of endothelial NOS (eNOS) in regulat-ing cardiac contractile function and diastolic function and playing othe physiological and pathophysiological roles.[