IMPAIRED RENORENAL REFLEXES IN 2-KIDNEY, ONE CLIP HYPERTENSIVE RATS
IMPAIRED RENORENAL REFLEXES IN 2-KIDNEY, ONE CLIP HYPERTENSIVE RATS
复制标题
DOI：
10.1161/01.hyp.14.4.445
复制
发表时间：
1989-10-01
期刊：
影响因子：
8.3
通讯作者：
BUCKLEYBLEILER, RL
中科院分区：
文献类型：
--
作者：
KOPP, UC;BUCKLEYBLEILER, RL
在血压正常的大鼠中，通过增加输尿管压力刺激肾机械感受器导致对侧抑制性肾肾反射反应和对侧尿钠排泄。通过用0.9 M NaCl灌注肾盂刺激肾化学感受器产生类似的效果。然而，在自发性高血压大鼠的肾反射反应的肾脏机械和化学感受器刺激受损。本研究旨在探讨两肾一夹高血压大鼠的肾反射是否发生了改变，这是一种高血压模型，其中肾传入神经参与了外周交感神经活动的增强。在研究前4周，将0.2 mm银夹放置在一根肾动脉周围。在研究时，平均动脉压为156 . ±.。4毫米汞柱。肾机械感受器和化学感受器刺激的nonclipped或clipped肾脏未能影响同侧传入肾神经活动，对侧传出神经活动，对侧尿流率和尿钠排泄。非夹闭肾脏的肾脏去神经使同侧尿钠排泄量从0.65 .+-增加。0.13到1.50 .+-. 0.42μ mol/min/g，并且对侧尿钠排泄从0.18 ± 0.15 μ mol/min/g降低。0.03至0.13 ±。0.03μ mol/min/g（p < 0.05）。因此，去神经的nonclipped肾导致类似的对侧兴奋性肾肾反射反应，在血压正常的大鼠。然而，去神经切断肾脏增加了同侧和对侧尿钠排泄，从0.14 ± 0.15。0.04至0.27 . ±. 0.5μ mol/min/g和从1.29 ±. 0.33至2.09 .+-。0.59μ mol/min/g（p < 0.01）。总之，这些数据表明，缺乏抑制性肾肾反射从夹肾可能会增加传出交感神经活动，从而有助于高血压大鼠的两肾，一夹。
In normotensive rats, stimulation of renal mechanoreceptors by an increase in ureteral pressure results in a contralateral inhibitory renorenal reflex response with contralateral natriuresis. Similar effects are produced by stimulation of renal chemoreceptors by renal pelvic perfusion with 0.9 M NaCl. However, in spontaneously hypertensive rats the renorenal reflex responses to renal mechanoreceptor and chemoreceptor stimulation are impaired. The present study was performed to examine whether the renoremal reflexes were altered in two-kidney, one clip hypertensive rats, a model of hypertension in which it has been suggested that the afferent renal nerves contribute to the enhanced peripheral sympathetic nervous activity. A 0.2 mm silver clip was placed around one renal artery 4 weeks before the study. At the time of study, mean arterial pressure was 156 .+-. 4 mm Hg. Renal mechanoreceptor and chemoreceptor stimulation of either the nonclipped or clipped kidney failed to affect ipsilateral afferent renal nerve activity, contralateral efferent nerve activity, and contralateral urine flow rate and urinary sodium excretion. Renal denervation of the nonclipped kidney increased ipsilateral urinary sodium excretion from 0.65 .+-. 0.13 to 1.50 .+-. 0.42 .mu.mol/min/g and decreased contralateral urinary sodium excretion from 0.18 .+-. 0.03 to 0.13 .+-. 0.03 .mu.mol/min/g (p < 0.05). Thus, denervation of the nonclipped kidney resulted in a similar contralateral excitatory renorenal reflex response as in normotensive rats. However, denervation of the clipped kidney increased both ipsilateral and contralateral urinary sodium excretion, from 0.14 .+-. 0.04 to 0.27 .+-. 0.5 .mu.mol/min/g and from 1.29 .+-. 0.33 to 2.09 .+-. 0.59 .mu.mol/min/g (p < 0.01), respectively. Taken together these data suggest that the lack of inhibitory renorenal reflexes from the clipped kidney may enhance efferent sympathetic nervous activity and thereby contribute to the hypertension in two-kidney, one clip hypertensive rats.