We examined whether nitric oxide (NO) and ATP take part in inhibitory nonadrenergic, noncholinergic (NANC) neurotransmission in the portal vein of Japanese White rabbits. Longitudinal strips of the vein were suspended in organ baths containing Krebs bicarbonate solution. Preparations relaxed in response to electrical field stimulation (EFS) (25 V, 0.5 msec in duration, 1-50 Hz) and exogenous ATP (1-300 microM) after contraction was induced with 10 microM ergotamine in the presence of 3 microM guanethidine and 0.1 microM atropine. 2. The relaxation response to EFS was abolished by addition of 100 microM NG-nitro-L-arginine, an NO synthase inhibitor. This abolition was partly reversed by 10 mM L-arginine, a substrate for NO synthase. 3. The relaxation response to exogenous ATP was significantly inhibited by 1 mM suramin, a P2X- and P2Y-purinoceptor antagonist, whereas relaxation response to EFS was not inhibited by 1 mM suramin. 4. From the results of this study, we conclude that the inhibitory NANC neurotransmission is mediated by NO alone and does not involve ATP in the portal vein of Japanese White rabbits under our experimental conditions.
摘要
我们研究了一氧化氮(NO)和三磷酸腺苷(ATP)是否参与日本白兔门静脉的抑制性非肾上腺素能、非胆碱能(NANC)神经传递。将静脉的纵行条带悬挂于含有 Krebs 碳酸氢盐溶液的器官浴槽中。在用 10 μM 麦角胺在 3 μM 胍乙啶和 0.1 μM 阿托品存在下诱导收缩后,制备物对电场刺激(EFS)(25 V,持续时间 0.5 毫秒,1 - 50 Hz)和外源性 ATP(1 - 300 μM)产生松弛反应。2. 添加 100 μM NO 合酶抑制剂 NG - 硝基 - L - 精氨酸可消除对 EFS 的松弛反应。这种消除被 10 mM L - 精氨酸(NO 合酶的底物)部分逆转。3. 1 mM 苏拉明(一种 P2X 和 P2Y 嘌呤受体拮抗剂)显著抑制对外源性 ATP 的松弛反应,而 1 mM 苏拉明不抑制对 EFS 的松弛反应。4. 根据本研究结果,我们得出结论,在我们的实验条件下,日本白兔门静脉的抑制性 NANC 神经传递仅由 NO 介导,不涉及 ATP。