Potassium load prevents the decrease of GFR induced by captopril in sodium-depleted rats.
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 F1 alpha (PGF1 alpha) and thromboxane B2 (TxB2). Urinary kallikrein-like activity (UKALLV) and plasma aldosterone increased in K-loaded animals. LNC rats had lower clearances of inulin (CIN) and p-aminohippurate (CPAH) 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 less than 0.01). KCl-loaded LNC rats had CIN and CPAH greater than LNC (0.64 +/- 0.16 and 1.90 +/- 0.28 ml.min-1.100 g body wt-1, P less than 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 CIN from 0.49 +/- 0.09 to 0.30 +/- 0.08 ml.min-1.100 g body wt-1 (P less than 0.01). Aprotinin did not affect renal function despite significant decrease of UKALLV. 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.
Rathaus
M
M
Department of Nephrology, Meir Hospital, Kfar Saba, Israel.
Pomeranz
A
A
Podjarny
E
E
Bernheim
J
J
D000450:Aldosterone / Q000097:blood; D000818:Animals; D002216:Captopril / Q000494:pharmacology*; D002712:Chlorides / Q000494:pharmacology; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects*; D007444:Inulin / Q000378:metabolism; D007610:Kallikreins / Q000652:urine; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D011188:Potassium / Q000494:pharmacology* / Q000652:urine; D011453:Prostaglandins / Q000096:biosynthesis; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000172:deficiency*; D010130:p-Aminohippuric Acid / Q000378:metabolism
D002712:Chlorides; D011453:Prostaglandins; D000450:Aldosterone; D007444:Inulin; D002216:Captopril; D012964:Sodium; D007610:Kallikreins; D011188:Potassium; D010130:p-Aminohippuric Acid