Fleming I, Busse R
Institut für Kardiovaskuläre Physiologie, Klinikum der J.W. Goethe-Universität, Frankfurt am Main, Germany.
J Mol Cell Cardiol. 1999 Jan;31(1):5-14. doi: 10.1006/jmcc.1998.0839.
Since the discovery of an endothelium-derived relaxing factor (EDRF) by Furchgott and Zawadzki (Furchgott and Zawadzki. 1980), which was later identified as nitric oxide (NO) (Ignarro et al., 1987; Palmer et al., 1987; Furchgott, 1988), it has become clear that there are a number of additional endothelium-derived vasodilator and vasoconstrictor autacoids (endothelin-1, prostaglandin H2, and the endothelium-derived hyperpolarizing factor: EDHF). None of these autacoids play such a central role in the regulation of vascular tone and homeostasis as the primary EDRF, the free radical NO, which is generated via a live-electron oxidation of a guanidino nitrogen from L-arginine by an NO synthase (NOS).
自弗奇戈特和扎瓦茨基发现内皮源性舒张因子(EDRF)(弗奇戈特和扎瓦茨基,1980年)以来,该因子后来被鉴定为一氧化氮(NO)(伊格纳罗等人,1987年;帕尔默等人,1987年;弗奇戈特,1988年),现已明确还存在许多其他内皮源性血管舒张和血管收缩自分泌物质(内皮素-1、前列腺素H2以及内皮源性超极化因子:EDHF)。这些自分泌物质在血管张力和内环境稳态的调节中,均不像主要的内皮源性舒张因子——自由基NO那样发挥核心作用。自由基NO是由一氧化氮合酶(NOS)通过L-精氨酸胍基氮的活电子氧化作用生成的。