血管紧张素II在大鼠对躯体神经刺激的肾脏反应中的作用。

The role of angiotensin II in the renal responses to somatic nerve stimulation in the rat.

作者信息

Handa R K, Johns E J

机构信息

Department of Physiology, Medical School, Birmingham.

出版信息

J Physiol. 1987 Dec;393:425-36. doi: 10.1113/jphysiol.1987.sp016831.

DOI:10.1113/jphysiol.1987.sp016831

PMID:3328780

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1192401/

Abstract

Electrical stimulation of the brachial nerves at 3 Hz (15 V, 0.2 ms), in sodium pentobarbitone-anaesthetized rats whose renal arterial pressure was held constant, elicited a 26% increase in systemic blood pressure, a 15% rise in heart rate, an 11% reduction in renal blood flow, did not alter glomerular filtration rate and significantly reduced absolute and fractional sodium excretions and urine flow by 44, 49 and 31%, respectively. 2. In a separate group of rats, brachial nerve stimulation at 3 Hz increased plasma renin activity approximately 2-fold, while in animals in which the brachial nerves were not stimulated plasma renin activity did not change. 3. Following inhibition of the renin-angiotensin system with captopril or sar-1-ile-8-angiotensin II, brachial nerve stimulation resulted in similar increases in systemic blood pressure and heart rate as in the animals with an intact renin-angiotensin system but, in captopril-infused rats, did not change renal haemodynamics or urine flow while absolute and fractional sodium excretions were reduced by 20 and 25%, respectively. In sar-1-ile-8-angiotensin II-infused animals, similar nerve stimulation decreased renal blood flow by 12%, glomerular filtration rate by 7% and absolute and fractional sodium excretions and urine flow by 25, 18 and 18%, respectively. These decreases in sodium and water output were significantly smaller than those observed in animals with an intact renin-angiotensin system. 4. Stimulation of the brachial nerves increased post-ganglionic efferent renal nerve activity by 20% and the magnitude of this response was unaffected following inhibition of the renin-angiotensin system. 5. The results show that low rates of brachial nerve stimulation in the rat can increase efferent renal nerve activity and result in an antinatriuresis and antidiuresis which is dependent on the presence of angiotensin II, and appears to be due to an action of angiotensin II at the level of the kidney.

摘要

在肾动脉血压保持恒定的戊巴比妥钠麻醉大鼠中，以3 Hz（15 V，0.2 ms）的频率电刺激臂神经，可使全身血压升高26%，心率升高15%，肾血流量减少11%，肾小球滤过率未改变，绝对和分数钠排泄量及尿流量分别显著降低44%、49%和31%。2. 在另一组大鼠中，3 Hz的臂神经刺激使血浆肾素活性增加约2倍，而未刺激臂神经的动物血浆肾素活性未改变。3. 用卡托普利或Sar-1-Ile-8-血管紧张素II抑制肾素-血管紧张素系统后，臂神经刺激导致的全身血压和心率升高与肾素-血管紧张素系统完整的动物相似，但在输注卡托普利的大鼠中，肾血流动力学和尿流量未改变，而绝对和分数钠排泄量分别降低20%和25%。在输注Sar-1-Ile-8-血管紧张素II的动物中，类似的神经刺激使肾血流量降低12%，肾小球滤过率降低7%，绝对和分数钠排泄量及尿流量分别降低25%、18%和18%。这些钠和水排出量的降低明显小于肾素-血管紧张素系统完整的动物。4. 刺激臂神经使节后肾传出神经活动增加20%，抑制肾素-血管紧张素系统后该反应的幅度未受影响。5. 结果表明，大鼠中低频率的臂神经刺激可增加肾传出神经活动，并导致钠利尿和利尿作用减弱，这依赖于血管紧张素II的存在，且似乎是由于血管紧张素II在肾脏水平的作用。