Renal prostaglandins and sodium balance in the rabbit: lack of effect of aspirin-like drugs.

Urinary prostaglandin E2 (PGE2) and PGF2 excretion was previously found to be inversely related to sodium intake in the rabbit. Renal prostaglandin (PG) synthesis might therefore be involved in the renal handling of sodium. This possibility was tested by studying sodium excretion during inhibition of renal PG synthesis with four different nonsteroidal anti-inflammatory drugs in unanaesthetized, female rabbits. The rabbits n = 5-6) were kept in metabolic cages and chronically maintained on different sodium containing diets. On a medium salt diet (0.4% NaCl), neither treatment with indomethacin (1.5 mg/kg x 2 or 3 mg/kg x 2) nor diclofenac (1.5 mg/kg x 2) for three days changed the urinary excretion of sodium and water although the mean excretion of immunoreactive PGE2 (iPGE2) and iPGF2 were reduced by between 43-78%. On a very low salt diet (0.05% NaCl), two days treatment with aspirin (30 mg/kg x 2), diclofenac (3 mg/kg x 2), indomethacin (3.5 mg/kg x 2) or naproxen (10 mg/kg x 2) did not alter sodium excretion in any significant direction. The mean urinary PGE2 and PGF2 excretion was reduced by 35-63% and 63-85%, respectively. These results do not support a major role of PGs in the chronic regulation of sodium balance in the rabbit. The possible influence of mineralocorticoids on renal PG synthesis was studied by administration of aldosterone (100 microgram/kg x 2) for two days to rabbits on a high salt diet (2% NaCl) and cancrenoate (10 mg/kg x 2), an aldosterone antagonist, to rabbits on the very low salt diet. However, neither drug significantly changed the urinary excretion of PGF2 alpha, indicating that renal PG synthesis is not influenced by mineralocorticoids in the rabbit.