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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 synthase (NOS) catalyzes the oxidation of L-arginine to form L-citrulline and nitric oxide (NO). Its product NO can exert its complex physiological functions through cGMP (cGMP) -dependent and cGMP-independent pathways, such as maintaining vascular tone, regulating blood pressure, inhibiting vascular smooth muscle cell migration, proliferation and inhibiting platelet aggregation in the cardiovascular system Leukocyte adhesion to the vascular wall and regulation of myocardial contraction and diastolic function, and participate in the regulation of heart rate variability. In this paper, three kinds of NOS isozymes genes and their gene expression regulation and influencing factors are briefly reviewed. The mechanisms of cardiac autonomic regulation of nNOS1, inhibition of cardiac contractility by iNOS, and cardioprotection and injury are emphasized. The mechanisms involved in the regulation of eNOS in cardiac function and other physiological and pathological aspects are reviewed.