Pohl U, de Wit C
Johannes Gutenberg University, Institute of Physiology, Mainz.
Pflugers Arch. 1996;432(3 Suppl):R107-10.
Since the early observations of Carl Ludwig that the sympathetic nervous system exerts a tonic influence on resistance vessels, many additional factors have been identified which control vascular tone. The active modulator role of endothelium-derived nitric oxide (NO) in this process has emerged only in the last decade. The interaction of the local vasodilator, NO, with systemic alpha-adrenergic control of vascular tone as well as with pressure-induced myogenic vasoconstriction is briefly reviewed in the present paper. Cellular mechanisms of this interaction are discussed. In vitro and in vivo experiments indicate that the continuous basal release of NO potently attenuates alpha-adrenergic and myogenic tone in resistance vessels by several independent mechanisms and that endothelial impairment results in abnormal vasoconstriction.
自从卡尔·路德维希早期观察到交感神经系统对阻力血管施加紧张性影响以来，已发现许多其他控制血管张力的因素。内皮衍生的一氧化氮（NO）在此过程中的积极调节作用仅在过去十年才得以显现。本文简要回顾了局部血管舒张因子NO与血管张力的全身α-肾上腺素能控制以及压力诱导的肌源性血管收缩之间的相互作用。讨论了这种相互作用的细胞机制。体外和体内实验表明，NO的持续基础释放通过几种独立机制有效减弱阻力血管中的α-肾上腺素能和肌源性张力，并且内皮损伤会导致异常血管收缩。
