Renal Prostaglandins and Sodium Balance in the Rabbit: Lack of Effect of Aspirin‐like Drugs

Abstract

Urinary prostaglandin [PG] E2 and PGF2 excretion is inversely related to Na intake in the rabbit. Renal PG synthesis might therefore be involved in the renal handling of Na. This possibility was tested by studying Na excretion during inhibition of renal PG synthesis with 4 different nonsteroidal anti-inflammatory drugs in unanesthetized, female rabbits. The rabbits (n = 5-6) were kept in metabolic cages and chronically maintained on different Na containing diets. On a medium salt diet (0.4% NaCl), neither treatment with indomethacin (1.5 mg/kg .times. 2 or 3 mg/kg .times. 2) nor declofenac (1.5 mg/kg .times. 2) for 3 days changed the urinary excretion of Na and H2O although the mean excretion of immunoreactive [i] PGE2 and iPGF2 were reduced by between 43-78%. On a very low salt diet (0.05% NaCl), 2 days treatment with aspirin (30 mg/kg .times. 2), diclofenac (3 mg/kg .times. 2), indomethacin (3.5 mg/kg .times. 2) or naproxen (10 mg/kg .times. 2) did not alter Na excretion in any significant direction. The mean urinary PGE2 and PGF2 excretion was reduced by 35-63% and 63-85%, respectively. These results apparently do not support a major role of PG in the chronic regulation of Na balance in the rabbit. The possible influence of mineralocorticoids on renal PG synthesis was studied by aldosterone administration (100 .mu.g/kg .times. 2) for 2 days to rabbits on a high salt diet (2% NaCl) and cancrenoate (10 mg/kg .times. 2), an aldosterone antagonist, to rabbits on a very low salt diet. Neither drug significantly changed urinary PGF2.alpha. excretion indicating that renal PG synthesis apparently is not influenced by mineralocorticoids in the rabbit.