Bloch W, Addicks K, Hescheler J, Fleischmann B K
Institut I für Anatomie, Universität zu Köln, 50931 Köln, Federal Republic of Germany.
Microsc Res Tech. 2001 Nov 15;55(4):259-69. doi: 10.1002/jemt.1175.
Nitric oxide (NO) is an important signalling molecule that plays a relevant role in different cell systems, among them the adult heart. The effects of NO are primarily mediated through modulation of Ca(2+) homeostasis, myofibrillar contractility, and metabolic regulation in cardiomyocytes. Recent evidence also suggests an important role of NO for cardiomyogenesis by modulating proliferation and differentiation and regulating cardiac function. In the embryonic, but also the healthy and diseased, adult mammalian heart, the inducible (iNOS) and the endothelial (eNOS) nitric oxide synthases (NOS) are detected. However, the expression pattern of NO and its function differ during development. Furthermore, under pathophysiological conditions NOS expression can also change and cause impairment of cardiac performance and cytotoxic effects. The present review focuses on the role and function of NO during cardiomyogenesis, the mechanisms responsible for eNOS availability, and the paracrine effects of NO generated by cardiomyocytes.
一氧化氮（NO）是一种重要的信号分子，在不同的细胞系统中发挥着相关作用，其中包括成年心脏。NO的作用主要通过调节心肌细胞中的Ca(2+)稳态、肌原纤维收缩性和代谢调节来介导。最近的证据还表明，NO通过调节增殖和分化以及调节心脏功能，在心肌生成中发挥重要作用。在胚胎期以及健康和患病的成年哺乳动物心脏中，均可检测到诱导型（iNOS）和内皮型（eNOS）一氧化氮合酶（NOS）。然而，NO的表达模式及其功能在发育过程中有所不同。此外，在病理生理条件下，NOS表达也会发生变化，导致心脏功能受损和细胞毒性作用。本综述重点关注NO在心肌生成过程中的作用和功能、负责eNOS可用性的机制以及心肌细胞产生的NO的旁分泌作用。
