卡托普利对肾血管性高血压大鼠近远期降压的机理

The Antihypertensive Mechanism of Captopril on Renovascular Hypertensive RatS in Acute and Chronic Phases

应用二肾一夹型肾血管性高血压大鼠（２ＫｌＣ－ＲＨＲ）模型，观察在高血压稳定期血小板胞浆内钙离子浓度（［ＦＣａ２＋］ｉ）、血小板聚集率及血浆ＡⅡ的变化，在此基础上研究血管紧张素转化酶抑制剂一卡托普利不同给药阶段的作用。发现近期实验虽然显著降低血压，血浆ＡⅡ减少，但血小板内［Ｃａ２＋］ｉ，血小板聚集率没有变化；远期实验在显著降低血压的同时血小板内［Ｃａ２＋］ｉ、血小板聚集率明显减少（Ｐ＜０．０１）。提示２ＫｌＣ－ＲＨＲ在高血压稳定期存在细胞内钙离子代谢异常和血小板活性的改变，血小板活性的降低可能参与卡托普利的远期降压作用。

To evaluate the effects and mechanism of Capto pril on the BP of 2-kidney,1-clip renovascular hypertensive rats (2KlC-RHR) in the two phases (acute and chronic phase,respecticely),we measure platelets cytosolic free calcium concentration([Ca2+]i),platelets aggregation(PAg) and plasma angiotensin Ⅱ(AⅡ)levels. The results are as follows:(1)captopril reduce the BP significantly while A Ⅱ level decrease in the acute phase,with no changes in [Ca2 +]i and PAg;(2)Captopril has obvious antihypertension in the chronic phase,with [Ca2+]i and PAg decreasing markedly.In conclusion,the results indicate that there are abnormality of the intracellular calcium and platelets activity during the sustain period of hypertension in the 2KlC-RHR, the antihypertension effect of Captopril during the chronic phase may partly be attributed to its inhibition effect on platelets activity.