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

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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.

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