Radomski M W, Palmer R M, Moncada S
Wellcome Research Laboratories, Beckenham, Kent, U.K.
Biochem Biophys Res Commun. 1987 Nov 13;148(3):1482-9. doi: 10.1016/s0006-291x(87)80299-1.
The inhibition of platelet adhesion by nitric oxide (NO) and prostacyclin and their mechanism of action was studied. Platelet adhesion to collagen fibrils and endothelial cell matrix was inhibited completely by NO but only partially by prostacyclin. Adhesion of platelets to endothelial cell monolayers was inhibited by bradykinin. This effect of bradykinin was unaffected by aspirin, and was accounted for by the amounts of NO released by the endothelial cells. Inhibition of platelet adhesion by NO and prostacyclin was potentiated by selective inhibitors of cGMP phosphodiesterase, but not of cAMP phosphodiesterase, indicating that elevation of cGMP regulates platelet adhesion.
研究了一氧化氮(NO)和前列环素对血小板黏附的抑制作用及其作用机制。NO可完全抑制血小板与胶原纤维和内皮细胞基质的黏附,而前列环素只能部分抑制。缓激肽可抑制血小板与内皮细胞单层的黏附。缓激肽的这种作用不受阿司匹林的影响,且由内皮细胞释放的NO量所介导。cGMP磷酸二酯酶选择性抑制剂可增强NO和前列环素对血小板黏附的抑制作用,而cAMP磷酸二酯酶选择性抑制剂则无此作用,这表明cGMP升高可调节血小板黏附。