AJP - Renal AJP: Lung Cellular and Molecular Physiology
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Am J Physiol Renal Physiol 260: F170-F176, 1991;
0363-6127/91 $5.00
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AJP - Renal Physiology, Vol 260, Issue 2 170-F176, Copyright © 1991 by American Physiological Society


ARTICLES

Stimulation of renin release by hyperkalemia in the nonfiltering kidney

H. B. Lin, D. B. Young and M. J. Smith Jr
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.

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.





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