中文摘要：

目的研究热应激改变肾动脉、肠系膜动脉、股动脉血管平滑肌“肾上腺素受体的反应性。方法将大鼠置于高温环境，使直肠温度升至42℃，持续15min，从而制作热应激模型。热应激后48h，用敏感的离体血管张力描记技术记录大鼠肾动脉、肠系膜动脉、股动脉血管的张力，用实时定量的反转录聚核酶链反应技术测定动脉平滑肌的mRNA水平，研究d受体反应性改变的机制。结果热应激后，肾动脉a肾上腺素受体介导的收缩量效曲线明显右移，pD2值由对照组的6．97±0．05降低为5．68±0．08，最大收缩能力由对照组的（146±12）％增强为（230±24）％；肠系膜动脉a肾上腺素受体介导的收缩量效曲线无明显改变；股动脉仪肾上腺素受体介导的收缩敏感性增加，量效曲线明显左移。热应激后肾动脉d1受体的mRNA水平增高，a2受体的mRNA水平与对照组差异无统计学意义；肠系膜动脉、股动脉a1受体及a2受体mRNA水平与对照组差异无统计学意义。结论热应激后，肾动脉a受体敏感性降低，股动脉a受体敏感性增加，引起血流的重新分配，提示热应激延迟预适应有肾脏保护效应。

英文摘要：

Objective To investigate the responsiveness change of renal, mesenterie and femoral artery a-adrenergic receptor following heat stress in rats. Methods The heat stress model was constructed by positioning the rats in an environment with increased temperature, thus rendering an elevated rectal temperature to 42 ℃ for 15 min. At 48 h, the myograph recording technique that sensitively captured the isometric tension of renal, mesenterie and femoral artery in vitro was employed and real-time quantitative polymerase chain reaction was applied to determine the mechanism regarding changes ofa- adrenergic receptor mRNA expression. Two groups, namely the heat stress group （n=14） and control group （n=14）, were set in the study. Results The heat stress resulted in a substantial right shift of the a- adrenergic receptor mediated concentration-contractile curve for the renal artery. Compared with control group, heat stress group was associated with a significantly reduced pDz value [ （5.68±0.08） vs （6.97±0.05） ] and augmented maximal contraction [ （230±24）% vs （146± 12）% 1. The a adrenergic receptor-mediated concentration- contractile curve of mesenteric artery was not considerably altered. Heat stress led to an increased a-adrenergic receptor contractile sensitivity and marked left shift of the concentration-contractile curve of femoral artery. Heat stress yielded augmented adrenergic receptor, but not a2-adrenergic receptor, mRNA expression in the renal artery compared with control group. The differences inal- anda2-adrenergic receptor mRNA expression in mesenteric and femoral artery were unremarkable compared with control group. Conclusions Heat stress reduces the sensitivity of a-adrenergic receptor in renal artery, which is augmented in femoral artery. The resultant redistribution of blood flow suggests that the preconditioning phenomenon delayed by heat stress may confer renal protective effects.