大鼠肾脏钙排泄神经调节的研究。

An investigation into the neural regulation of calcium excretion by the rat kidney.

作者信息

Johns E J, Manitius J

机构信息

Department of Physiology, Medical School, Birmingham.

出版信息

J Physiol. 1987 Feb;383:745-55. doi: 10.1113/jphysiol.1987.sp016439.

DOI:10.1113/jphysiol.1987.sp016439

PMID:3656142

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1183100/

Abstract

An investigation was undertaken to examine the action of the renal nerves on the reabsorption of calcium ions from the left kidney of sodium pentobarbitone anaesthetized rats. 2. Renal denervation had no effect on renal haemodynamics but increased urine flow, calcium excretion, absolute and fractional sodium excretions by 26% (P less than 0.02), 73% (P less than 0.02), 90% (P less than 0.001) and 82% (P less than 0.01), respectively, without affecting the calcium to sodium excretion ratio. In a group of animals which were similarly prepared but the renal nerves were not sectioned, neither renal blood flow, nor the excretion of water, calcium or sodium changed during the time course of the experiment although glomerular filtration rate increased significantly (P less than 0.05) by 19%. 3. Low rates (0.8-1.5 Hz at 15 V, 0.2 ms) of renal nerve stimulation did not change renal haemodynamics but reduced urine flow by 31% (P less than 0.001), calcium excretion by 32% (P less than 0.001), sodium excretion by 32% (P less than 0.001) and fractional sodium excretion by 32% (P less than 0.01) while the calcium to sodium excretion ratio was unaffected. Renal nerve stimulation at 3-5 Hz reduced renal blood flow by 15% (P less than 0.02), did not change glomerular filtration rate and reduced urine flow, calcium excretion, absolute and fractional sodium excretions by 35% (P less than 0.01), 30% (P less than 0.01), 32% (P less than 0.01) and 32% (P less than 0.05), respectively, while the calcium to sodium excretion ratio remained unchanged. 4. These data show that the renal nerves can modulate the excretion of calcium by a mechanism which is independent of renal haemodynamics and which may represent a direct action of the nerves on the calcium reabsorptive processes of the tubular cells. It remains to be determined whether this neural control of calcium reabsorption is a direct one or indirect via changes in sodium reabsorption.

摘要

开展了一项研究，以检查肾神经对戊巴比妥钠麻醉大鼠左肾钙离子重吸收的作用。2. 肾去神经支配对肾血流动力学没有影响，但分别使尿量、钙排泄量、绝对钠排泄量和分数钠排泄量增加了26%（P<0.02）、73%（P<0.02）、90%（P<0.001）和82%（P<0.01），而不影响钙钠排泄比。在一组同样制备但未切断肾神经的动物中，在实验过程中肾血流量、水、钙或钠的排泄均未改变，尽管肾小球滤过率显著增加（P<0.05）了19%。3. 低频率（15V、0.2ms时0.8 - 1.5Hz）的肾神经刺激未改变肾血流动力学，但使尿量减少了31%（P<0.001），钙排泄量减少了32%（P<0.001），钠排泄量减少了32%（P<0.001），分数钠排泄量减少了32%（P<0.01），而钙钠排泄比未受影响。3 - 5Hz的肾神经刺激使肾血流量减少了15%（P<0.02），未改变肾小球滤过率，并分别使尿量、钙排泄量、绝对钠排泄量和分数钠排泄量减少了35%（P<0.01）、30%（P<0.01）、32%（P<0.01）和32%（P<0.05），而钙钠排泄比保持不变。4. 这些数据表明，肾神经可通过一种独立于肾血流动力学的机制调节钙排泄，这可能代表神经对肾小管细胞钙重吸收过程的直接作用。钙重吸收的这种神经控制是直接的还是通过钠重吸收的变化间接实现的，仍有待确定。