腺苷受体激动剂对大鼠离体主动脉的作用及其机制

Effects and mechanisms of adenosine receptor agonists in rat isolated aorta

目的 研究不同腺苷受体 (A R)激动剂对大鼠离体主动脉环的作用及其机制。方法 分别给予A2 R激动剂CPCA和A1 R激动剂CPA ,观察离体主动脉环对 0 6 2 μmol·L-1去甲肾上腺素的反应 ,并观察它们的作用是否依赖于血管内皮、细胞外钙和ATP敏感性钾通道 (KATP)。结果 5 0 μmol·L-1CPCA可引起血管扩张 ,去除血管内皮或换用无钙营养液后此作用消失 ,KATP阻滞剂格列苯脲并不能阻断CPCA的血管扩张作用。CPA在 10 μmol·L-1浓度时不引起血管扩张 ,10 0 μmol·L-1浓度时有血管扩张作用 ,此作用在去除内皮后或换用无钙营养液后仍然存在 ,格列苯脲不能阻断此作用。结论 CPCA引起主动脉的扩张依赖于血管内皮和细胞外钙的存在 ,高浓度CPA则通过直接作用于平滑肌细胞而引起血管扩张 ,KATP均不参与A

AIM To analyze the vasodilator effects of adenosine receptor agonists in the rat isolated aorta, explore the relationship between adenosine receptor agonists and adenosine triphosphate sensitive potassium channel(K ATP ), and probe its mechanisms. METHODS Effects of 5 ( N cyclopropyl) carboxamidoadenosine(CPA), an adenosine A 2 receptor agonist ,and N 6 cyclopentyladenosine(CPCA),an adenosine A 1 receptor agonist, on norepinephrine induced vasoconstriction were observed in the isolated rings of aorta. RESULTS 50 μmol·L -1 of CPCA produced a vasodilator effect in isolated aorta.This effect could be abolished without endothelium or extracellular calcium. K ATP blocker glibencalmide could not block the vasodilation induced by CPCA.On the other hand,100 μmol·L -1 of CPA caused a relatively weak vasodilator effect.This effect could not be blocked by 10 μmol·L -1 of glibenclamide also,but still existed without endothelium or extracellular calcium. CONCLUSION CPCA induced vasodilation dependent endothelium and extracellular calcium, but CPA causes vasodilation through vascular smooth muscle. These relaxations could not be blocked by 10 μmol·L -1 of glibenclamide.