Activation of endothelial guanylate cyclase inhibits cellular reactivity.

R Heller, F Bussolino, D Ghigo, G P Pescarmona, R Calvino, A Gasco, U Till, A Bosia
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引用次数: 9

Abstract

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.

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活化内皮鸟苷酸环化酶抑制细胞反应性。
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,可被硝普钠(SNP)、SIN-1 (3- morpholinosydnon亚胺)和S35b(4-甲基-3-苯基磺酰基呋喃嘧啶)激活。用这些化合物预处理的细胞显示出抑制凝血素诱导的花生四烯酸释放、PGI2形成、PAF合成和PMNL粘附的作用。内皮鸟苷环化酶也可以被一氧化氮(NO)激活,一氧化氮是由内皮细胞在凝血酶或离子霉素刺激下产生的。提示内源性NO可能通过cgmp依赖机制控制细胞活化和内皮功能。
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