Giménez José, García M Paz, Serna Mar, Bonacasa Bárbara, Carbonell Luis F, Quesada Tomás, Hernández Isabel
Department of Physiology, Faculty of Medicine, University of Murcia, Murcia, Spain.
Exp Physiol. 2006 Jul;91(4):715-22. doi: 10.1113/expphysiol.2006.033449. Epub 2006 Apr 20.
The objective of this study was to investigate whether the acute haemodynamic effects of angiotensin-converting enzyme inhibition with captopril could be enhanced by oestrogen administration, and then to evaluate the mechanisms involved in this enhancement. All experiments were performed in 18-week-old female spontaneously hypertensive rats arranged in three experimental groups: intact; ovariectomized (OVX); and ovariectomized plus treatment with 17beta-oestradiol (OVX + E2). These groups were used to evaluate the effects of captopril administration alone, or following bradykinin B2 receptor blockade or nitric oxide synthase inhibition, on a number of haemodynamic parameters (mean arterial pressure, cardiac index, vascular resistance and heart rate). The drop in mean arterial pressure and vascular resistance index in response to captopril was more pronounced in intact and ovariectomized rats treated with 17beta-oestradiol than in ovariectomized animals. Blockade of bradykinin B2 receptors or inhibition of nitric oxide synthesis attenuated the synergy between 17beta-oestradiol and captopril. It is concluded that ovariectomy blunted the blood pressure and vascular resistance index drop observed in intact rats in response to captopril. Treatment with 17beta-oestradiol prevented the blunted response to captopril in ovariectomized rats. Kinins and nitric oxide may be involved in the mechanisms of 17beta-oestradiol potentiation of the haemodynamic effects of captopril.
本研究的目的是调查给予雌激素是否能增强卡托普利抑制血管紧张素转换酶的急性血流动力学效应,进而评估这种增强作用所涉及的机制。所有实验均在18周龄的雌性自发性高血压大鼠身上进行,这些大鼠被分为三个实验组:完整组;卵巢切除组(OVX);卵巢切除加17β-雌二醇治疗组(OVX + E2)。这些组用于评估单独给予卡托普利,或在缓激肽B2受体阻断或一氧化氮合酶抑制后,对一些血流动力学参数(平均动脉压、心脏指数、血管阻力和心率)的影响。与卵巢切除的动物相比,给予17β-雌二醇的完整组和卵巢切除组大鼠对卡托普利反应时平均动脉压和血管阻力指数的下降更为明显。缓激肽B2受体阻断或一氧化氮合成抑制减弱了17β-雌二醇与卡托普利之间的协同作用。研究得出结论,卵巢切除减弱了完整大鼠对卡托普利反应时观察到的血压和血管阻力指数下降。给予17β-雌二醇可防止卵巢切除大鼠对卡托普利的反应减弱。激肽和一氧化氮可能参与了17β-雌二醇增强卡托普利血流动力学效应的机制。