Blockade of AT1 receptors enhances baroreflex control of heart rate in conscious rabbits with heart failure.
Blockade of AT1 receptors enhances baroreflex control of heart rate in conscious rabbits with heart failure.
复制标题
阻断 AT1 受体可增强心力衰竭清醒兔子心率的压力反射控制。
DOI：
10.1152/ajpregu.1996.271.1.r303
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Zucker,IH
中科院分区：
文献类型：
--
作者：
Murakami,H;Liu,JL;Zucker,IH
由于肾素-血管紧张素系统在心力衰竭中被激活，我们假设血管紧张素II（ANG II）在心力衰竭环境中改变压力反射敏感性中起作用。因此，我们评估了压力反射控制的心率（HR）在清醒的，慢性仪器家兔在正常状态下和建立心力衰竭后。以360-380次/min的速率快速心室起搏诱导心力衰竭，平均持续14.5 +/- 1.4天。将数据与以类似方式装备的正常家兔进行比较。压力感受性反射曲线通过在腔静脉和主动脉弓上植入液压封堵器或通过给予苯肾上腺素和硝普钠来产生。在静脉内施用AT 1拮抗剂L-158，809之前和之后进行实验。心力衰竭兔的动脉压显著降低（81 +/- 3 vs. 69 +/- 4 mmHg，P < 0.05），静息心率升高（230 +/- 5 vs. 260 +/- 10次/分，P < 0.05），左房压升高（3.6 +/- 0.7 vs. 13.1 +/- 0.7 mmHg，P < 0.05）。血管紧张素Ⅱ阻断对正常家兔的静息或压力反射参数几乎没有影响。然而，在心力衰竭家兔中，L-158，809主要通过增加压力感受器激活期间诱发的最小HR来增强压力感受器反射敏感性（2.7 ± 0.5 vs.4.7 ± 0.8 beats.min-1.mmHg-1; P < 0.05）。在心力衰竭家兔中，L-158，809给药后，β 1-阻滞剂对任何压力反射参数均无影响。然而，L-158，809可显著降低心力衰竭家兔阿托品预处理后的最低HR。这些数据表明，ANG II在该心力衰竭模型中心脏交感神经张力的调节中起作用，并且可能是心力衰竭中观察到的压力反射敏感性降低的原因。
Because the renin-angiotensin system is activated in heart failure, we hypothesized that angiotensin II (ANG II) plays a role in altering baroreflex sensitivity in the setting of heart failure. Accordingly, we evaluated the baroreflex control of heart rate (HR) in conscious, chronically instrumented rabbits in the normal state and after the establishment of heart failure. Heart failure was induced by rapid ventricular pacing at a rate of 360-380 beats/min for an average of 14.5 +/- 1.4 days. The data were compared with normal rabbits instrumented in a similar fashion. Baroreflex curves were generated by inflation of implanted hydraulic occluders on the vena cava and aortic arch or by administration of phenylephrine and sodium nitroprusside. Experiments were carried out before and after intravenous administration of the AT1 antagonist L-158,809. Rabbits with heart failure exhibited significantly lower arterial pressure (81 +/- 3 vs. 69 +/- 4 mmHg, P < 0.05), elevated resting HR (230 +/- 5 vs. 260 +/- 10 beats/min, P < 0.05), and elevated left atrial pressure (3.6 +/- 0.7 vs. 13.1 +/- 0.7 mmHg, P < 0.05). ANG II blockade had little effect on resting or baroreflex parameters in normal rabbits. However, in rabbits with heart failure, L-158,809 enhanced baroreflex sensitivity (2.7 +/- 0.5 vs. 4.7 +/- 0.8 beats.min-1.mmHg-1; P < 0.05), primarily by increasing the minimum HR evoked during baroreceptor activation. beta 1-Blockade had no effect on any baroreflex parameter after L-158,809 in rabbits with heart failure. However, L-158,809 significantly reduced the minimum HR after pretreatment with atropine in rabbits with heart failure. These data suggest that ANG II plays a role in modulation of cardiac sympathetic tone in this model of heart failure and may be responsible for the depressed baroreflex sensitivity observed in heart failure.