Relationship between adenosine-induced vascular effects and ATP-sensitive K+ channels.

H M He, H Wang, W B Xiao
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Abstract

Aim: To study the relationship between adenosine (Ade) receptors and adenosine 5'-triphosphate (ATP)-sensitive potassium (KATP) channels in rat aorta.

Methods: Isolated rat aorta rings were suspended for isometric force recording. The vascular effects of Ade were assessed in the presence or absence of functional endothelium. The interactions of Ade and pinacidil (Pin) or glibenclamide (Gli) were investigated.

Results: In isolated aorta preconstricted with KCl 20 mmol.L-1, Ade 3-300 mumol.L-1 induced relaxation in a concentration-dependent manner; and in 48/99 preparations from 32 rats, Ade induced initial transient constriction followed by sustained relaxation. When the functions of KATP channels were blocked with Gli 1 or 100 mumol.L-1, effects of Ade were characterized by vasoconstriction rather than vasorelaxation. The combination of Pin 1 mumol.L-1 with Ade 100 mumol.L-1 showed no synergic vasodilatory effects and did not affect Ade-induced vasoconstriction. After the removal of endothelium, Ade still induced vasoconstriction and vasorelaxation, and the constrictive effects showed no difference from those in the presence of endothelium, but the potency of vasodilatory effects became weaker with slower decrease in tension.

Conclusion: The activation of KATP channels is involved in Ade receptor-induced vasodilation.

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腺苷诱导的血管效应与atp敏感K+通道的关系。
目的:研究大鼠主动脉腺苷(Ade)受体与腺苷5′-三磷酸(ATP)敏感钾(KATP)通道的关系。方法:取离体大鼠主动脉环悬吊进行等距力记录。在有无功能内皮的情况下评估Ade对血管的影响。研究了Ade与平酸酯(Pin)或格列本脲(Gli)的相互作用。结果:KCl 20 mmol预缩离体主动脉。L-1, Ade 3-300 μ mol。L-1诱导弛豫呈浓度依赖性;在32只大鼠的48/99个制剂中,Ade诱导最初的短暂收缩,随后持续松弛。当Gli 1或100 μ mol阻断KATP通道功能时。L-1, Ade的作用以血管收缩而非血管松弛为特征。引脚1 mumol的组合。L-1加Ade 100 μ mol。L-1无协同血管舒张作用,不影响ade诱导的血管收缩。去内皮后,Ade仍能诱导血管收缩和舒张,收缩效果与有内皮时无明显差异,但血管舒张效果减弱,张力下降速度减慢。结论:KATP通道的激活参与了Ade受体诱导的血管舒张。
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