Effect of cardiac receptor stimulation on renal vascular resistance in the pregnant rat.

Effect of cardiac receptor stimulation on renal vascular resistance in the pregnant rat.
复制标题

心脏受体刺激对妊娠大鼠肾血管阻力的影响。

DOI:
10.1152/ajpregu.2000.278.1.r171
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发表时间:
2000
期刊:
American journal of physiology. Regulatory, integrative and comparative physiology
影响因子:
--
通讯作者:
Herzer,WA
Herzer,WA
中科院分区:
--
文献类型:
--
作者:
Hines,T;Herzer,WA

文献摘要

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与处女相比,怀孕大鼠的心脏受体(CR)刺激会导致平均动脉压(MAP)反射性降低。由于 CR 介导的交感抑制对肾脏有优先影响,因此我们测试了妊娠期间肾血管阻力 (RVR) 是否因 CR 刺激而变化较小,并研究了可能的机制。通过向心房分级注射生理盐水来测量麻醉动物对 CR 刺激的反应,测量 MAP、右心房压力、肾交感神经活动 (RSNA)、肾血流量 (RBF) 和 RVR。与处女大鼠相比,妊娠晚期大鼠的基线 MAP 和 RVR 以及 CR 刺激期间这些变量的反射变化减少(P < 0.05)。妊娠大鼠中 RSNA 的反射变化减弱,但两组中 RBF 作为 RSNA 函数的变化相似。 ANG II AT1 受体阻断更能增加原始大鼠的基础 RBF(P < 0.05),但 AT1 阻断后 MAP、RSNA 和 RVR 反射变化的组间差异得以维持。因此,在 CR 模拟过程中,怀孕大鼠的 RVR 反射变化比处女大鼠有所减少。这种差异似乎并不涉及 ANG II 的差异效应。
Stimulation of cardiac receptors (CR) evokes blunted reflex reductions in mean arterial pressure (MAP) in pregnant compared with virgin rats. Because CR-mediated sympathoinhibition has preferential effects on the kidney, we tested whether, during pregnancy, renal vascular resistance (RVR) changes less in response to CR stimulation and investigated possible mechanisms. MAP, right atrial pressure, renal sympathetic nerve activity (RSNA), renal blood flow (RBF), and RVR were measured in anesthetized animals in response to CR stimulation by graded atrial injections of saline. Baseline MAP and RVR and reflex changes in these variables during CR stimulation were reduced in late-pregnant vs. virgin rats (P< 0.05). Reflex changes in RSNA were attenuated in pregnant rats, but changes in RBF as a function of RSNA were similar in both groups. ANG II AT1-receptor blockade increased basal RBF more in virgin rats (P< 0.05), but between-group differences in reflex changes in MAP, RSNA, and RVR were maintained after AT1blockade. Thus during CR simulation, reflex changes in RVR were reduced in pregnant versus virgin rats. This difference does not appear to involve differential effects of ANG II.