1. The synthesis of prostaglandin (PG) E2, PGF2α, 6-keto-PGF1α 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 hyponatremia, lost weight and their creatinine clearance decreased.
3. The glomerular synthesis of PGE2, PGF2α and 6-keto-PGF1α, but not of TXB2, was significantly increased in LNa rats. In LNa-CEI rats, the synthesis of PGE2 and 6-keto-PGF1α was similar to control values, but PGF2α and TXB2 synthesis was elevated at day 9. In cortical tubules, PGE2 and PGF2α were unaffected by Na+ depletion, but 6-keto-PGF1α 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 PGF2α, but not of 6-keto-PGF1α and TXB2, was significantly depressed. In inner medulla, Na+ depletion only tended to decrease PGF2α and 6-keto-PGF1α, but in the presence of captopril, the synthesis of all prostanoids was significantly decreased.