Li J M, Fenton R A, Cutler B S, Dobson J G
Division of Vascular Surgery, University of Massachusetts Medical School, Worcester 01655, USA.
Am J Physiol. 1995 Aug;269(2 Pt 1):C519-23. doi: 10.1152/ajpcell.1995.269.2.C519.
Adenosine per se is a potent vasodilator of vascular smooth muscle. Endothelial cells modulate vascular tone via the release of nitric oxide (NO), which also elicits vasodilation. This study was undertaken to determine whether adenosine could directly stimulate endothelial cells to enhance NO production, which could subsequently reduce vascular tone. NO production was evaluated in porcine carotid artery endothelial cells (PCAEC) and human saphenous vein endothelial cells (HSVEC) seeded on multiwell plates, grown to confluence, and treated with adenosine for 1 h. The bathing medium was collected, and the NO production was determined as reflected by the formation of NO2- and NO3-. NO production by PCAEC was significantly increased by adenosine in a dose-dependent manner, whereas there was only an insignificant tendency for an increase by HSVEC. The addition of the NO synthase competitive inhibitor, NG-monomethyl-L-arginine (NMMA), or the adenosine receptor antagonist, theophylline, prevented the increase in NO production by adenosine. The results suggest that adenosine stimulates, by a receptor-mediated mechanism, the production of NO by arterial, but not by venous, endothelial cells.
腺苷本身是血管平滑肌的一种强效血管扩张剂。内皮细胞通过释放一氧化氮（NO）来调节血管张力，NO也会引起血管舒张。本研究旨在确定腺苷是否能直接刺激内皮细胞以增强NO生成，进而降低血管张力。在接种于多孔板上、生长至汇合状态并经腺苷处理1小时的猪颈动脉内皮细胞（PCAEC）和人隐静脉内皮细胞（HSVEC）中评估NO生成。收集孵育培养基，并通过NO2-和NO3-的形成来测定NO生成量。PCAEC的NO生成量随腺苷浓度升高呈显著剂量依赖性增加，而HSVEC仅呈现出不显著的增加趋势。添加NO合酶竞争性抑制剂NG-单甲基-L-精氨酸（NMMA）或腺苷受体拮抗剂茶碱可阻止腺苷引起的NO生成增加。结果表明，腺苷通过受体介导机制刺激动脉内皮细胞而非静脉内皮细胞产生NO。
