Effect of potassium depletion on renin release

R. G. Luke, R. H. Lyerly, J. Anderson, J. H. Galla, T. A. Kotchen

Research output: Contribution to journalArticlepeer-review

Abstract

To study the mechanism of hyperreninemia that is induced by potassium depletion (KD), we examined renin responses to baroreceptor and macula densa stimuli in control and potassium-depleted rats. Potassium depletion was induced by dietary potassium deprivation and deoxycorticosterone acetate (DOCA) administration and was confirmed by depletion of muscle potassium. Plasma renin activity (PRA) and renal renin content (RRC) were elevated in unanesthetized potassium-depleted rats as compared to controls (PRA 7.5 ± 1.7 vs. 3.6 ± 0.6 ng/ml/hr, P<0.01; RRC 663 ± 127 vs. 415 ± 56 U/kidney, P<0.01). During progressive arterial hemorrhage, PRA rose significantly and similarly in potassium depletion (14.1 ± 2.2 to 39.8 ± 10.3) and control (8.9 ± 0.7 to 29.4 ± 5.4) rats. Acute sodium chloride (150 mEq/liter) infusion and selective chloride depletion, produced by peritoneal dialysis against NaHCO3 (150 mEq/liter) and followed by plasma volume expansion with salt-free bovine serum albumin (BSA), are macula densa stimuli. PRA failed to be suppressed in potassium-depleted rats (11.8 ± 2.9 to 12.3 ± 3.3; P-NS) in response to acute sodium chloride infusion, unlike controls (9.4 ± 1.7 to 4.6 ± 1.1; P<0.005) and failed to rise after acute selective chloride depletion (37 ± 2 to 45 ± 5; P = NS), also unlike controls (18 ± 3 to 57 ± 3; P<0.001). We conclude that potassium depletion induces selective inhibition of the responses to macula densa stimuli for renin release and suggest that potassium depletion-induced hyperreninemia may be due to the inhibition of a tonic suppressive macula densa signal that is dependent in control rats on normal chloride transport in the thick ascending limb of Henle's loop.

Original languageEnglish (US)
Pages (from-to)14-19
Number of pages6
JournalUnknown Journal
Volume21
Issue number1
DOIs
StatePublished - 1982

ASJC Scopus subject areas

  • Nephrology

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