Schmidt K, Werner E R, Mayer B, Wachter H, Kukovetz W R
Institut für Pharmakodynamik und Toxikologie, Universität Graz, Austria.
Biochem J. 1992 Jan 15;281 ( Pt 2)(Pt 2):297-300. doi: 10.1042/bj2810297.
Inhibition of tetrahydrobiopterin (H4biopterin) biosynthesis in endothelial cells almost completely abolished the agonist-induced formation of endothelium-derived relaxing factor (EDRF) (NO). This inhibitory effect could be antagonized when H4biopterin biosynthesis was restored by activating a salvage pathway. These data indicate that the formation of EDRF strictly depends on the presence of intracellular H4biopterin, which, in addition to Ca2+, may represent a further physiological and/or pathophysiological regulatory of endothelial NO synthases.
抑制内皮细胞中四氢生物蝶呤（H4biopterin）的生物合成几乎完全消除了激动剂诱导的内皮源性舒张因子（EDRF，即NO）的生成。当通过激活补救途径恢复H4biopterin生物合成时，这种抑制作用可被拮抗。这些数据表明，EDRF的生成严格依赖于细胞内H4biopterin的存在，除了Ca2+之外，H4biopterin可能代表内皮型一氧化氮合酶的另一种生理和/或病理生理调节因素。
