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目的探讨Urocortin(Ucn)对自发性高血压大鼠(SHR)胸主动脉舒缩功能的作用及机制.方法采用体外血管灌流,观察Ucn对SHR胸主动脉的舒张作用,以及左旋硝基精氨酸甲酯(N(ω)n itro-L-argin ine methyl ester,L-NAME)、亚甲蓝(M ethylene B lue,MB)和格列本脲(G lybenc lam ide)对其舒张作用的影响.结果Ucn(1 nmol.L-1~1μmol.L-1)可明显舒张内皮完整和去内皮SHR胸主动脉(P“,”Aim To investigate the vasodilatory effect and the mechanisms of urocortin(Ucn) on the thoracic aorta of spontaneously hypertensive rats(SHR).Methods Rings cut from SHR thoracic aorta were used in vitro.The endothelium dependent and independent vasorelaxing effects of Ucn were measured.Furthermore,it was also explored whether the relaxing effects of Ucn were affected by N(ω) nitro-L-arginine methyl ester(L-NAME), methylene blue(MB) and glybenclamide.Results Ucn(1 nmol·L-1~1 μmol·L-1) caused concentration dependent relaxation in SHR thoracic aorta with endothelium and without endothelium(P<0.01);L-NAME(100 μmol·L-1),the inhibitor of NOS and methylene blue(10 μmol·L-1),the inhibitor of GTP-cyclase,partly blocked the Ucn-induced relaxation of SHR thoracic aorta.Glybenclamide(10 μmol·L-1),the ATP-sensitive potassium channel inhibitor,also inhibited the Ucn-induced relaxation.Conclusion These findings suggest that Ucn can relax SHR thoracic aorta in endothelium dependent and independent manner.The vasodilatory effect of Ucn is partly achieved via activating the excretion of NO.Moreover,the vasorelaxing effect of Ucn is associated with NO-cGMP pathway and KATP channels.