Potassium load prevents the decrease of GFR induced by captopril in sodium-depleted rats

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Abstract

Captopril decreases the glomerular filtration rate (GFR) in Na-depleted rats and inhibits the stimulation of glomerular prostanoid synthesis induced by Na depletion. Because K loading stimulates glomerular prostanoid production in normal rats, we studied the effects of K loading in Na-depleted captopril-treated (LNC) rats. Potassium, but not Cl, loading stimulated the glomerular synthesis of 6-ketoprostaglandin F(1α) (PGF(1α)) and thromboxane B2 (TxB2). Urinary kallikrein-like activity (U(KALL)V) and plasma aldosterone increased in K-loaded animals. LNC rats had lower clearances of inulin (C(IN)) and p-aminohippurate (C(PAH)) than controls (0.22 ± 0.02 vs. 0.94 ± 0.07 and 0.56 ± 0.12 vs. 2.23 ± 0.23 ml · min-1 100 g body wt-1, both P < 0.01). KCl-loaded LNC rats had C(IN) and C(PAH) greater than LNC (0.64 ± 0.16 and 1.90 ± 0.28 ml · min-1 · 100 g body wt-1, P < 0.01). Similar results were observed in LNC rats loaded with a K solution not containing Cl, but not in LNC rats loaded with a mixture of CaCl2, MgCl2, and HCl. In KCl-loaded LNC rats, cyclooxygenase inhibition decreased C(IN) from 0.49 ± 0.09 to 0.30 ± 0.08 ml · min-1 · 100 g body wt-1 (P < 0.01). Aprotinin did not affect renal function despite significant decrease of U(KALL)V. We conclude that K loading prevents the decrease of GFR induced by captopril in Na-depleted rats and that this might be mediated by stimulation of glomerular prostanoid synthesis.

Original languageEnglish
Pages (from-to)F670-F674
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume258
Issue number3 27-3
DOIs
StatePublished - 1990
Externally publishedYes

Keywords

  • kallikrein
  • prostaglandin E
  • prostaglandin I
  • renal failure
  • thromboxane

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