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Influence of enalapril on established pressure-overload cardiac hypertrophy in low and normal renin states in female rats.

机译:依那普利对雌性大鼠低肾素和正常肾素状态下已建立的压力超负荷心肌肥大的影响。

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To determine whether effects of angiotensin converting enzyme (ACE) inhibitors on well-established pressure overload-induced cardiac hypertrophy and coronary remodeling depend upon normal plasma renin levels, the influence of enalapril on ventricular mass and coronary vascular resistance (CVR) was determined in a low-renin female rat model of chronic pressure overload, (deoxycorticosterone acetate hypertension, DOCA), and compared to its effect in a normal-renin model, (aortic construction, AC). Six weeks after experiment initiation, plasma renin activity of DOCA-treated rats was reduced to approximately 12% that of sham-treated and AC-treated groups. Enalapril was then added to the drinking water of half the animals in each group for two additional weeks. Comparing experimental groups to controls, this delayed enalapril treatment had 1) no effect on the elevated arterial pressures, 2) no effect on the elevated coronary resistance, and, in the DOCA group, 3) no effect on cardiac hypertrophy. However, this brief enalapril treatment reduced absolute and relative ventricular weights of AC rats. These data suggest that circulating renin is required for the anti-hypertrophic efficacy of late-onset brief treatment with enalapril. Since enalapril-induced reversal of cardiac hypertrophy in AC rats was not accompanied by reversal of coronary remodeling, growth signals other than angiotensin II may be involved in coronary remodeling.
机译:为了确定血管紧张素转化酶(ACE)抑制剂对良好建立的压力超负荷引起的心脏肥大和冠状动脉重塑的影响是否取决于正常血浆肾素水平,在临床试验中确定了依那普利对心室质量和冠状动脉血管阻力(CVR)的影响。慢性压力超负荷(醋酸脱氧皮质酮高血压,DOCA)的低肾素雌性大鼠模型,并与正常肾素模型(主动脉构造,AC)中的作用进行比较。实验开始六周后,经DOCA处理的大鼠的血浆肾素活性降低至假治疗和AC治疗组的约12%。然后将依那普利加入每组一半动物的饮用水中,持续另外两个星期。将实验组与对照组进行比较,这种延缓的依那普利治疗对1)升高的动脉压没有影响,2)对升高的冠状动脉阻力没有影响,在DOCA组中3)对心脏肥大没有影响。然而,这种短暂的依那普利治疗减少了AC大鼠的绝对和相对心室重量。这些数据表明循环肾素是依那普利晚期发作短暂治疗的抗肥厚功效所必需的。由于依那普利诱发的AC大鼠心脏肥大逆转并未伴随冠状动脉重构逆转,因此除血管紧张素II以外的其他生长信号可能参与了冠状动脉重构。

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