论文部分内容阅读
内皮型与神经型一氧化氮合酶(eNOS,nNOS)在心肌细胞内持续表达,而细胞应激可引起诱导型NOS(iNOS)表达。心肌细胞结构型eNOS与nNOS源性NO,在生理条件下对心肌主要发挥4方面的抑制作用:减缓心肌细胞搏动频率,轻度抑制心肌细胞收缩功能,加速心肌细胞舒张并增加顺应性,以及轻度抑制线粒体电子传递而增强氧利用效率。在生理条件下动员心肌储备与心肌肥厚时,与细胞膜上受体形成复合体的eNOS,其分泌的NO通过适度的抑制作用,调和受体介导的信号,形成类似于增强性拮抗的作用;与RyR形成复合体的nNOS源性NO,经抑制作用而稳定RyR钙释放功能,并增加肌质网钙离子转运效率。在心肌缺血-再灌注损伤或心力衰竭条件下,除上述eNOS和nNOS源性NO发挥的作用外,iNOS源性NO则主要通过抑制线粒体的电子传递,防止线粒体可通透转化孔的开放。由上述研究结果可见,无论在生理还是病理条件下,NO呈现出多种适度抑制作用,从而发挥心肌保护作用。
Endothelial and neuronal nitric oxide synthase (eNOS, nNOS) are consistently expressed in cardiomyocytes, whereas cellular stress induces iNOS expression. Myocardial cell-structure eNOS and nNOS-derived NO mainly exert inhibitory effects on myocardium under physiological conditions in four aspects: slowing down the frequency of cardiomyocytes pulsation, mildly inhibiting cardiomyocyte contractile function, accelerating cardiomyocyte relaxation and increasing compliance, and light Inhibition of mitochondrial electron transport enhances oxygen utilization efficiency. When physiological myocardium reserve and myocardial hypertrophy were mobilized under physiological conditions, eNOS secreted by complexing with receptors on cell membrane could mediate the receptor - mediated signal through modest inhibition and formed a similar effect as enhanced antagonism. The nNOS-derived NO, which forms a complex with RyR, stabilizes RyR calcium release by inhibition and increases sarcoplasmic reticulum Ca2 + transport efficiency. In the condition of myocardial ischemia-reperfusion injury or heart failure, iNOS-derived NO prevents the opening of mitochondrial transmembrane pore through the inhibition of electron transport of mitochondria, except for the role of eNOS and nNOS-derived NO. From the above results, no matter in physiological or pathological conditions, NO showed a variety of moderate inhibition, which play a role in myocardial protection.