论文部分内容阅读
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 R激动剂的扩血管作用
Objective To study the effects of different adenosine receptor (A R) agonists on isolated aortic rings of rats and its mechanism. Methods The A2 R agonist CPCA and A1 R agonist CPA were given respectively to observe the response of isolated aortic rings to 0 6 2 μmol·L-1 norepinephrine and to observe whether their effects depend on the vascular endothelium and extracellular Calcium and ATP-sensitive potassium channels (KATP). Results 50 μmol·L-1 CPCA induced vasodilation. The effect disappeared after removal of vascular endothelium or replacement with calcium-free nutrient solution. Glibenclamide did not block the vasodilatation of CPCA. CPA did not cause vasodilatation at a concentration of 10 μmol·L-1, vasodilatation was observed at a concentration of 10 μmol·L-1, and this effect remained after the removal of endothelial cells or replacement with calcium-free nutrient solution. Can not block this effect. Conclusions CPCA induced the expansion of the aorta dependent on the presence of vascular endothelium and extracellular calcium. High concentrations of CPA caused vasodilatation through direct action on smooth muscle cells, and KATP did not participate in the vasodilator effect of A R agonist