Afferent pathways in cardiovascular adjustments induced by volume expansion in anesthetized rats
Afferent pathways in cardiovascular adjustments induced by volume expansion in anesthetized rats
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DOI：
10.1152/ajpregu.2000.279.3.r884
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发表时间：
2000-09-01
影响因子：
2.8
通讯作者：
Cravo, RL
中科院分区：
文献类型：
--
作者：
Colombari, BSA;Colombari, E;Cravo, RL
在麻醉大鼠中研究了压力感受器、心肺感受器和肾神经在4% Ficoll（Pharmacia; 1%体重，0.4 ml/min）容量扩张（VE）的心血管调节中的作用。在对照组动物中，VE导致平均动脉压（MAP）短暂升高，在10分钟时达到峰值（17 +/- 4 mmHg），肾血管传导性（10分钟和40分钟时分别为基线的128 +/- 6和169 +/- 19%）和后肢血管传导性（143 +/- 6和150 +/- 10%）升高。这些心血管调节VE不受双侧迷走神经切断术的影响。去窦弓神经后，VE诱导的MAP增加大于对照组大鼠（30 +/- 4 mmHg）。然而，肾血管舒张反应VE被阻断，而后肢血管舒张是类似于在对照组大鼠中观察到的。单侧肾去神经后（血流记录同侧），最初的肾血管舒张被阻断。然而，VE后40分钟，出现了显著的肾血管舒张（125 +/- 4%）。后肢血管舒张和MAP反应不受肾脏去神经支配的影响。这些结果表明，压力感受器传入是心血管调节VE的重要组成部分，特别是在控制肾血管传导。他们还表明，肾血管舒张引起的VE是由神经和激素机制介导的。
The role of baroreceptors, cardiopulmonary receptors, and renal nerves in the cardiovascular adjustments to volume expansion (VE) with 4% Ficoll (Pharmacia; 1% body wt, 0.4 ml/min) were studied in urethan-anesthetized rats. In control animals, VE produced a transitory increase in mean arterial pressure (MAP), which peaked at 10 min (17 +/- 4 mmHg) and increases in renal (128 +/- 6 and 169 +/- 19% of baseline at 10 and 40 min, respectively) and hindlimb vascular conductance (143 +/- 6 and 150 +/- 10%). These cardiovascular adjustments to VE were unaffected by bilateral vagotomy. After sinoaortic denervation, the increase in MAP induced by VE was greater than in control rats (30 +/- 4 mmHg). However, renal vasodilation in response to VE was blocked, whereas hindlimb vasodilation was similar to that observed in control rats. After unilateral renal denervation (ipsilateral to flow recording), the initial renal vasodilation was blocked. However, 40 min after VE, a significant renal vasodilation (125 +/- 4%) appeared. The hindlimb vasodilation and MAP responses were unaffected by renal denervation. These results demonstrate that the baroreceptor afferents are an essential component of cardiovascular adjustments to VE, especially in the control of renal vascular conductance. They also suggest that renal vasodilation induced by VE is mediated by neural and hormonal mechanisms.