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目的探讨心血管系统不同分子组成的ATP敏感钾通道(KATP)在降低去窦弓神经(SAD)大鼠血压波动性(BPV)中的作用。方法建立SAD大鼠模型,利用计算机化清醒自由活动大鼠血流动力学监测技术,观察非选择性KATP开放剂吡那地尔、Kir6.1/Sur2B和Kir6.1/Sur1选择性开放剂二氮嗪对SAD大鼠BPV的影响;并观察用Kir6.1/Sur1选择性阻断剂5-羟基癸酸盐(5-HD)、Kir6.2/Sur2A选择性阻断剂HMR1098阻断KATP后,吡那地尔和二氮嗪对SAD大鼠BPV作用的改变。结果吡那地尔和二氮嗪能够降低SAD大鼠BPV(P<0.01),阻断Kir6.1/Sur1、Kir6.2/Sur2A后不改变吡那地尔和二氮嗪对BPV的降低作用。结论开放血管平滑肌细胞Kir6.1/Sur2B能够降低SAD大鼠的BPV。
Objective To investigate the role of ATP-sensitive potassium channel (KATP) in different cardiovascular components in reducing blood pressure fluctuation (BPV) in sinoaortic denervated rats. Methods A rat model of SAD was established. The hemodynamic monitoring technique was used to observe the effects of the selective open-label agents of pinacidil, Kir6.1 / Sur2B and Kir6.1 / Sur1, a nonselective KATP opener. Azadiazine on BPV in SAD rats was observed. After KATP was blocked by Kir6.1 / Sur1 selective blocker 5-hydroxydecanoate (5-HD) and Kir6.2 / Sur2A selective blocker HMR1098 , Pinacidil and diazoxide on the role of BPV in SAD rats. Results Pinacidil and diazoxide could reduce BPV in SAD rats (P <0.01). After blocking Kir6.1 / Sur1 and Kir6.2 / Sur2A, no effect of pinacidil and diazoxide on BPV was observed . Conclusion Open vessel smooth muscle cells (Kir6.1 / Sur2B) can reduce BPV in SAD rats.