胰岛素抵抗高血压大鼠血管舒张功能异常的机制  

The Mechanisms of Abnormal Vasorelaxation in Insulin Resistant \;Hypertensive Rats

作　　者：陈颜芳[1,2,3] 杨和平 韩启德[1,2,3] 

机构地区：[1]广东省心血管病研究所 [2]衡阳医学院分子生物学中心 [3]北京医科大学第三医院血管医学研究所

出　　处：《高血压杂志》1999年第2期183-186,共4页Chinese Journal of Hypertension

摘　　要：目的探讨胰岛素抵抗高血压（ＩＲＨ）大鼠血管舒张功能的改变及其可能机制。方法采用离体血管功能实验方法，观察大鼠主动脉的舒张功能及其平滑肌钙代谢功能；应用逆转录多聚酶链反应技术检测主动脉平滑肌Ｃａ２＋－ＡＴＰ酶ｍＲＮＡ的表达水平。结果（１）ＩＲＨ大鼠主动脉舒张速度减慢；（２）用无钙ｋｒｅｂｓ液灌流后苯肾上腺素引起的收缩反应显著低于对照大鼠；（３）ＩＲＨ大鼠主动脉平滑肌Ｃａ２＋－ＡＴＰ酶ｍＲＮＡ表达水平显著低于对照大鼠。结论ＩＲＨ大鼠主动脉舒张功能下降与Ｃａ２＋－ＡＴＰ基因酶ｍＲＮＡ水平表达下降引起的平滑肌Ｃａ２＋代谢功能障碍有关。Aim \ To investigate the changes of vascular relaxation function and the mechanisms involved in insulin resistant hypertension (IRH).\ Methods \ The characteristics of vascular relaxation and calcium metabolism were studied by functional experiments in rat aortae. The gene expression of Ca2+ATPase was studied by RTPCR.\ Results \ (1) Aortic relaxation was slower in IRH rats than that in normal rats. (2)After incubation of preparations with Ca2+free krebs for different periods, the reduction of phenylephrineinduced vasoconstriction was faster and more remarkable in IRH rats.(3) The expression level of Ca2+ATPase mRNA was lower in aorta isolated from IRH rats than that from normal rats. Conclusion \ The Ca2+pump dysfunction and abnormal Ca2+metabolism,which resulted from reduced Ca2+ATPase gene mRNA expression, might be the mechanisms involved in the abnormal vasorelaxation in the insulin resistant hypertensive rat model.

关 键 词：胰岛素抵抗 高血压 血管舒张 

分 类 号：R544.105[医药卫生—心血管疾病]