Effects of inhibitors of prostaglandin synthesis on renal sodium excretion in normal dogs and dogs with decreased renal mass

Abstract

The role of endogenous prostaglandins on Na excretion was studied. Na excretion was studied in awake, trained, normal dogs and dogs with reduced renal mass fed a fixed amount of NaCl (58 meq/day). Studies were performed under water diuresis or Na loading before and after administration of inhibitors of prostaglandin synthesis. In normal dogs undergoing a water diuresis fractional excretion of sodium (FENa) was 0.07 .+-. 0.01 before and 0.14 .+-. 0.03% after meclofenamate (values not significantly different). The effect of prostaglandin synthesis inhibitors on Na excretion, measured for 5 h after a 77 meq NaCl load given i.v., was studied in normal dogs and dogs with reduced renal mass. Normal dogs excreted 39.2 .+-. 9% of the Na load before and only 9.1 .+-. 1.6% after meclofenamate. This drug produced a similar decrease in Na excretion in dogs with reduced renal mass. Identical results were obtained with indomethacin in normal dogs and dogs with reduced renal mass. In awake dogs undergoing a water diuresis prostaglandin synthesis inhibitors do not affect Na excretion. When the same dogs were given a Na load, indomethacin or meclofenamate administration markedly decreased Na excretion. No significant changes in GFR [glomerular filtration rate] or renal blood flow occurred which would account for these observations. Prostaglandins, presumably of renal origin, play a key role in the natriuresis that follows the administration of modest Na loads.