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

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.