Li J m, Fenton R A, Wheeler H B, Powell C C, Peyton B D, Cutler B S, Dobson J G
Department of Surgery, University of Massachusetts Medical Center, Worcester, Massachusetts, 01655, USA.
J Surg Res. 1998 Dec;80(2):357-64. doi: 10.1006/jsre.1998.5439.
Adenosine is a potent vasodilator of vascular smooth muscle. Endothelium-derived nitric oxide (NO) elicits vasodilation. We have previously reported that adenosine stimulates the production of NO from porcine carotid arterial endothelial cells (PCAEC) via a receptor-mediated mechanism. This study was to determine whether adenosine also enhances NO production from human arterial endothelium and to define the involvement of adenosine A1 and A2 receptors.
Human iliac arterial endothelial cells (HIAEC) and PCAEC were harvested and cultured in dishes. NO production was evaluated with a NO electrode sensor which measured continuously real-time NO production.
NO content of the medium bathing HIAEC and PCAEC was significantly increased with adenosine (100 micromol/L). Ethylcarboxamidoadenosine (NECA), a nonselective adenosine receptor agonist, and carboxyethyl-phenethylamino-ethylcarboxamidoadenosine (CGS-21680), a selective adenosine A2a receptor agonist, increased NO production by HIAEC and PCAEC with respective EC50 values of 3.32 and 6.96 nmol/L for NECA and 30.97 and 29.47 nmol/L for CGS-21680. Chlorofuryl-triazolo-quinazolinamine (CGS-15943; 1 micromol/L), an adenosine A1 and A2 receptor antagonist, and aminofuryltriazolotriazinyl-aminoethylphenol (ZM-241385; 1 micromol/L), a selective adenosine A2a receptor antagonist, inhibited the effect of CGS-21680. Chlorocyclopentyl-adenosine (CCPA; 1 micromol/L), an adenosine A1 receptor agonist, significantly depressed NO production by both HIAEC and PCAEC: This effect was inhibited by cyclopentyl-dipropylxanthine (DPCPX), a selective adenosine A1 receptor antagonist.
The results demonstrate that adenosine A2a receptors increase, and adenosine A1 receptors decrease, the production of NO by human and porcine arterial endothelial cells.
腺苷是血管平滑肌的强效血管舒张剂。内皮衍生的一氧化氮（NO）可引起血管舒张。我们之前报道过，腺苷通过受体介导的机制刺激猪颈动脉内皮细胞（PCAEC）产生NO。本研究旨在确定腺苷是否也能增强人动脉内皮细胞产生NO，并确定腺苷A1和A2受体的参与情况。
收获人髂动脉内皮细胞（HIAEC）和PCAEC并培养于培养皿中。使用NO电极传感器评估NO的产生，该传感器可连续实时测量NO的产生。
用腺苷（100 μmol/L）处理后，HIAEC和PCAEC培养液中的NO含量显著增加。非选择性腺苷受体激动剂N-乙基羧基腺苷（NECA）和选择性腺苷A2a受体激动剂羧乙基苯乙氨基乙基羧基腺苷（CGS-21680）可增加HIAEC和PCAEC产生NO，NECA的EC50值分别为3.32和6.96 nmol/L，CGS-21680的EC50值分别为30.97和29.47 nmol/L。腺苷A1和A2受体拮抗剂氯呋喃基三唑并喹唑啉胺（CGS-15943；1 μmol/L）和选择性腺苷A2a受体拮抗剂氨基呋喃基三唑并三嗪基氨基乙基苯酚（ZM-241385；1 μmol/L）可抑制CGS-21680的作用。腺苷A1受体激动剂氯环戊基腺苷（CCPA；1 μmol/L）可显著降低HIAEC和PCAEC产生NO：该作用被选择性腺苷A1受体拮抗剂环戊基二丙基黄嘌呤（DPCPX）抑制。
结果表明，腺苷A2a受体增加，而腺苷A1受体减少人和猪动脉内皮细胞产生NO。
