Waldmann R, Walter U
Labor für Klinische Biochemie, Medizinische Universitätsklinik, Würzburg, F.R.G.
Eur J Pharmacol. 1989 Jan 17;159(3):317-20. doi: 10.1016/0014-2999(89)90165-9.
The mechanism of vasodilator-induced inhibition of platelet aggregation was investigated in human platelets. Cyclic nucleotide-elevating vasodilators stimulated cAMP- or cGMP-dependent protein phosphorylation, inhibited the activation of both protein kinase C and myosin light chain kinase, and inhibited the thrombin-induced hydrolysis of phosphatidylinositol-4,5-bisphosphate without affecting its resynthesis. The results suggest that cAMP- and cGMP-elevating vasodilators both inhibit platelet aggregation at an early step of the activation cascade, presumably at the level of phospholipase C.
在人血小板中研究了血管舒张剂诱导的血小板聚集抑制机制。升高环核苷酸的血管舒张剂刺激cAMP或cGMP依赖性蛋白磷酸化，抑制蛋白激酶C和肌球蛋白轻链激酶的激活，并抑制凝血酶诱导的磷脂酰肌醇-4,5-二磷酸水解，而不影响其再合成。结果表明，升高cAMP和cGMP的血管舒张剂均在激活级联反应的早期步骤抑制血小板聚集，可能是在磷脂酶C水平。
