Heller R, Bussolino F, Ghigo D, Pescarmona G P, Calvino R, Gasco A, Till U, Bosia A
Research Center of Vascular Biology and Medicine, University of Jena, Erfurt, FRG.
Agents Actions Suppl. 1995;45:177-81. doi: 10.1007/978-3-0348-7346-8_25.
The study shows that endothelial cells from human umbilical veins have a soluble guanylate cyclase which can be activated by sodium nitroprusside (SNP), SIN-1 (3-morpholinosydnonimine) and S35b (4-methyl-3-phenylsulfonylfuroxan). Cells which were pretreated with these compounds showed an inhibition of thrombin-induced arachidonic acid release, PGI2 formation, PAF synthesis and PMNL adhesion. Endothelial guanylate cyclase can also be activated by nitric oxide (NO) which is generated in endothelial cells upon stimulation with thrombin or ionomycin. It is suggested that endogenously produced NO might control cell activation and endothelial function through a cGMP-dependent mechanism.
研究表明，人脐静脉内皮细胞具有一种可溶性鸟苷酸环化酶，它可被硝普钠（SNP）、SIN-1（3-吗啉代亚硝酰）和S35b（4-甲基-3-苯基磺酰基呋咱）激活。用这些化合物预处理的细胞显示出凝血酶诱导的花生四烯酸释放、前列环素（PGI2）形成、血小板活化因子（PAF）合成及中性粒细胞黏附受到抑制。内皮鸟苷酸环化酶也可被一氧化氮（NO）激活，NO是内皮细胞在凝血酶或离子霉素刺激下产生的。提示内源性产生的NO可能通过环磷酸鸟苷（cGMP）依赖性机制控制细胞活化及内皮功能。
