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无滤过功能肾脏中高钾血症对肾素释放的刺激作用。

Stimulation of renin release by hyperkalemia in the nonfiltering kidney.

作者信息

Lin H B, Young D B, Smith M J

机构信息

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.

出版信息

Am J Physiol. 1991 Feb;260(2 Pt 2):F170-6. doi: 10.1152/ajprenal.1991.260.2.F170.

Abstract

This study was designed to analyze the acute effects of hyperkalemia on renin release in the normal filtering kidney and the nonfiltering kidney. Plasma K was increased by acute intravenous KCl infusion. In the normal filtering kidney experiment plasma K was 5.7 vs. 3.5 meq/l. Hyperkalemia resulted in a 45% increase in renal blood flow (RBF) and a 35% increase in glomerular filtration rate (GFR) at the 120-mmHg pressure level. Renin release was significantly greater in the hyperkalemic group than in the control group (P less than 0.01) with the greatest effect over the lower pressure range. In the nonfiltering kidney experiment plasma K was 6.09 vs. 3.5 meq/l. RBF was 33% greater in the hyperkalemic than in the normokalemic group at the 130-mmHg pressure level. Renin release was also greater in the hyperkalemic group than in the normokalemic group (P less than 0.01). However, unlike the normal filtering kidney experiments, in the nonfiltering kidneys the difference in renin release was most prominent at the highest level of renal perfusion pressure. These experiments demonstrate that acute hyperkalemia can cause renal vasodilation and stimulate renin release in both filtering and nonfiltering kidney preparations and that potassium may affect renin release both through a direct effect on the juxtaglomerular cells and indirectly by affecting delivery of fluid and/or NaCl to the macula densa.

摘要

本研究旨在分析高钾血症对正常滤过肾和非滤过肾中肾素释放的急性影响。通过急性静脉输注氯化钾使血浆钾升高。在正常滤过肾实验中,血浆钾为5.7 vs. 3.5 meq/l。在120 mmHg压力水平下,高钾血症导致肾血流量(RBF)增加45%,肾小球滤过率(GFR)增加35%。高钾血症组的肾素释放显著高于对照组(P小于0.01),在较低压力范围内影响最大。在非滤过肾实验中,血浆钾为6.09 vs. 3.5 meq/l。在130 mmHg压力水平下,高钾血症组的RBF比正常血钾组高33%。高钾血症组的肾素释放也高于正常血钾组(P小于0.01)。然而,与正常滤过肾实验不同,在非滤过肾中,肾素释放的差异在肾灌注压最高水平时最为显著。这些实验表明,急性高钾血症可导致肾血管舒张,并刺激滤过肾和非滤过肾制剂中的肾素释放,并且钾可能通过对球旁细胞的直接作用以及通过影响液体和/或NaCl向致密斑的输送间接影响肾素释放。

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