异丙肾上腺素舒血管作用机制的在体实验研究  

Study on the relationship between β-adrenoceptor and L-arginine/NO pathway in vivo

作　　者：李洁[1] 徐标[1] 何家声[1] 

机构地区：[1]南京铁道医学院附院心内科,江苏南京210009

出　　处：《中国病理生理杂志》2000年第9期842-844,共3页Chinese Journal of Pathophysiology

摘　　要：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 β2AIM and METHODS: A constant perfusion model of rabbit femoral artery was used to examine whether vasodilation induced by β-adrenoceptor(β-AR) stimulation is dependent on NOS activiation in vivo and which subtype(s) of β-AR is/are responsible for NOS activiation in order to ascertain the role of NO in vasodilation induced by β-AR stimulation. RESULTS: Isoprenaline elicited a concentration-dependent vasodilation of rabbit femoral artery, co-infusing NOS inhibitor L-NAME or β 2-AR antagonist ICI 118551 abolished the vasodilation by Isoprenaline, but β 1-AR antagonist CGP 20712A had no effect on vasodilation of rabbit femoral arterg induced by isoprenaline. CONCLUSION: Isoprenaline-induced vasodilation in this femoral vascular bed is mediated through activiation of NOS and only β 2-AR is responsible for this sort of vasodilation.

关 键 词：血管舒张 一氧化氮合酶 异丙肾上腺素 兔 

分 类 号：R972.4[医药卫生—药品]