论文部分内容阅读
目的观察硝基类扩血管药硝普钠（ｓｏｄｉｕｍｎｉｔｒｏｐｒｕｓｓｉｄｅ，ＳＮＰ）对卒中易感型自发高血压大鼠（ＳＨＲｓｐ）及其正常血压对照ＷＫＹ大鼠肠系膜动脉Ａ４－Ａ５分支阻力血管平滑肌钙激活钾通道（ＫＣａ）的作用。方法用细胞贴附式膜片箝（ｐａｔｃｈｃｌａｍｐ）技术。结果发现ＳＮＰ可激活ＳＨＲｓｐ与ＷＫＹ阻力血管平滑肌ＫＣａ在同等剂量（１ｎｍｏｌ／Ｌ）ＳＮＰ作用下，被激活的ＳＨＲｓｐＫＣａ的电导、通道开放电流等均小于正常对照ＷＫＹ大鼠。同等剂量（１０ｕｍｏｌ／Ｌ）的８－Ｂｒ－ｃＧＭＰ激活ＳＨＲｓｐＫＣａ的效应亦弱于ＷＫＹ，结果与ＳＮＰ激活作用相似。结论高血压时阻力血管平滑肌ＫＣａ对舒血管的血管内皮释放因子／一氧化氮（ＥＤＲＦ／ＮＯ）的反应减弱。
Objective To observe the effect of nitric oxide vasodilator SNP on the stroke-prone spontaneously hypertensive rats (SHRsp) and its normal blood pressure control (WKY), the A4-A5 branch of the mesenteric artery, and the vascular smooth muscle calcium-activated potassium channel (KCa) role. Methods Using patchclamp technique. The results showed that SNP activated SHRsp and WKY resistance vascular smooth muscle KCa under the same dose (1nmol / L) SNP, activated SHRspKCa conductance, channel opening current were smaller than the control WKY rats. The same dose (10umol / L) of 8-Br-cGMP activated SHRspKCa also weaker than the effect of WKY, the results and SNP activation similar. Conclusion The response of vascular smooth muscle KCa to vasorelaxant vascular endothelial cells releasing factor / nitric oxide (EDRF / NO) during hypertension is weakened.