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目的 :研究NOS(一氧化氮合酶 )抑制剂对异丙肾上腺素 (isoprenaline)产生的血管舒张作用的影响及涉及的 β -肾上腺素能受体 (β -AR)亚型 ,探讨NO是否作为 β -AR激动后信号转导过程中的信使物质参与 β -AR激动产生的血管舒张。 方法 :利用家兔股动脉恒流灌注模型。结果 :(1)Isoprenaline产生浓度依赖的血管舒张。 (2 )NOS抑制剂L -NAME阻断了isoprenaline产生的血管舒张作用。 (3) β1-AR阻滞剂CGP 2 0 712A不能阻断isoprenaline产生的外围血管舒张作用 ,但 β2 -AR阻滞剂ICI 1185 5 1能阻断isoprenaline产生的外周血管舒张作用。结论 :Isoprenaline引起兔股动脉舒张通过激活NOS介导 ,涉及的 β受体亚型为 β2 受体
AIM: To investigate the effect of nitric oxide synthase (NOS) inhibitors on vasodilatation induced by isoprenaline and the β-adrenergic receptor (β -AR) subtypes involved in this study. Messenger substances during signal transduction after β-AR activation participate in vasodilation induced by β-AR. Methods: The rabbit femoral artery perfusion model was used. Results: (1) Isoprenaline produced a concentration-dependent vasodilation. (2) The NOS inhibitor L-NAME blocks the vasodilatation produced by isoprenaline. (3) β1-AR blocker CGP 2 0 712A can not block peripheral vasodilatation induced by isoprenaline, but β2-AR blocker ICI 1185 5 1 can block peripheral vasorelaxation induced by isoprenaline. CONCLUSIONS: Isoprenaline-induced relaxation of the femoral artery in rabbits is mediated by activation of NOS, involving beta receptor subtypes as beta2 receptors