Effects of sodium depletion on renal prostanoid synthesis in rats: Influence of the converting enzyme inhibitor captopril

M. Rathaus, E. Podjarny, A. Pomeranz, J. Shapira, N. Kariv, J. Bernheim

Research output: Contribution to journalArticlepeer-review

Abstract

1. The synthesis of prostaglandin (PG) E2, PGF(2α), 6-keto-PGF(1α) and thromboxane (TX) B2 by isolated glomeruli, cortical tubules, inner medullary slices and outer medullary slices was measured in salt-depleted (LNa) rats and in salt-depleted rats receiving captopril (LNa-CEI). Animals were studied before and after 4, 9 and 15 days of Na+ depletion. 2. Na+ balance was reached in LNa rats after 4 days. Blood pressure and creatinine clearance remained stable. Serum Na+ decreased from 140 ± 1 to 126 ± 1 mmol/l (mean ± SEM, P < 0.01). In contrast, LNa-CEI rats were unable to conserve Na+ adequately: fractional excretion of Na+ and natriuresis were constantly greater than in LNa animals. As a consequence, LNa-CEI rats developed severe hyponatraemia, lost weight and their creatinine clearance decreased. 3. The glomerular synthesis of PGE2, PGF(2α) and 6-keto-PGF(1α), but not of TXB2 was significantly increased in LNa rats. In LNa-CEI rats, the synthesis of PGE2 and 6-keto-PGF(1α) was similar to control values, but PGF(2α) and TXB2 synthesis was elevated at day 9. In cortical tubules, PGE2 and PGF(2α) were unaffected by Na+ depletion, but 6-keto-PGF(1α) and TXB2 were increased and a similar trend was observed in LNa-CEI rats. In outer medulla of LNa rats, a decrease in all the eicosanoids measured was observed at day 4. In LNa-CEI animals, the synthesis of PGE2 and PGF(2α), but not of 6-keto-PGF(1α) and TXB2, was significantly depressed. In inner medulla, Na+ depletion only tended to decrease PGF(2α) and 6-keto-PGF(1α), but in the presence of captopril, the synthesis of all prostanoids was significantly decreased.

Original languageEnglish
Pages (from-to)469-474
Number of pages6
JournalClinical Science
Volume76
Issue number5
DOIs
StatePublished - 1989
Externally publishedYes

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