Fleming I, Busse R
Zentrum der Physiologie Klinikum, J. W. Goethe-Universität, Frankfurt/Main, Germany.
Adv Pharmacol. 1995;34:187-206. doi: 10.1016/s1054-3589(08)61086-8.
The intention of this chapter is to give a brief overview of the continuously expanding field of endothelium-derived NO. Over the past few years it has become apparent that the mechanisms controlling the activation of NOS are more complex than was previously thought, with factors such as pHi, [Ca2+]i, shear stress, and gender all contributing to the control of "basal" NO production as well as the regulation of NOS levels in endothelial cells. The list of the functional consequences of endothelial NO formation has also grown, with antiproliferative, antihypertensive, and antiatherogenic effects all being described. Recent advances at the molecular biology level have facilitated the pioneering of a whole new field of research, and a number of groups have shown that NO can modulate the expression of several genes, such as that encoding MCP-1, an effect that is probably due to an interaction between NO and transcription factors. Further elucidation of the signals that influence the production and actions of NO will, without doubt, further the understanding of numerous physiological and pathophysiological processes.
本章旨在简要概述内皮源性一氧化氮这一不断扩展的领域。在过去几年中，显而易见的是，控制一氧化氮合酶（NOS）激活的机制比之前认为的更为复杂，诸如细胞内pH值（pHi）、细胞内钙离子浓度（[Ca2+]i）、剪切应力和性别等因素，均对“基础”一氧化氮生成的控制以及内皮细胞中一氧化氮合酶水平的调节有所贡献。内皮一氧化氮生成的功能后果列表也在增加，已描述的包括抗增殖、抗高血压和抗动脉粥样硬化作用。分子生物学水平的最新进展推动了一个全新研究领域的开拓，许多研究小组表明，一氧化氮可调节多个基因的表达，例如编码单核细胞趋化蛋白-1（MCP-1）的基因，这种效应可能归因于一氧化氮与转录因子之间的相互作用。毫无疑问，进一步阐明影响一氧化氮生成和作用的信号，将加深对众多生理和病理生理过程的理解。
