The Renal Concentrating Defect Associated With Potassium Depletion Is Independent of Prostaglandin E2

R. M. Rosa*, F. H. Epstein, J. S. Stoff

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Prostalandin E2 (PGE2) impairs the hydrosmotic effect of vasopressin in toad bladder and mammalian kidney. Because some studies in animals have suggested that potassium depletion enhances renal PGE2 production, the present study examined whether the renal concentrating defect of potassium depletion in humans is mediated by PGE2. Five normal volunteers were studied before and after moderate potassium depletion achieved by 10 days of dietary potassium restriction and administration of a polystyrene sulfonate potassium exchange resin (Kayexalate). Maximal urinary osmolality (Umax) decreased from 1,094 ± 58 (mean ± SEM) to 820 ± 26 mmol/kg (mOsm/kg) (P < 0.01) following potassium depletion, but urinary PGE2 excretion did not change (496 ± 145 and 435 ± 186 ng/d, respectively). Indomethacin suppressed PGE2 excretion significantly, but failed to increase Umax in either the normal or the potassium-depleted state (1,094 ± 34 and 825 ± 56 mmol/kg, respectively). It is concluded that the renal concentrating defect produced by moderate potassium restriction in humans is not mediated by PGE2.

Original languageEnglish (US)
Pages (from-to)473-477
Number of pages5
JournalAmerican Journal of Kidney Diseases
Volume16
Issue number5
DOIs
StatePublished - 1990

Keywords

  • Antidiuretic hormone
  • indomethacin
  • potassium depletion
  • prostaglandins

ASJC Scopus subject areas

  • Nephrology

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