Effect of prostaglandin inhibition on renal response to volume expansion in dog

A prostaglandin (Pg) has been proposed as a “natriuretic hormone” effecting the natriuresis observed with extracellular fluid volume expansion. Dogs were volume expanded under chloralose anesthesia by equilibrating the animal's blood with the saline expanding volume outside of the body prior to infusion, in order to avoid hemodilution during expansion. The massive natriuresis associated with expansion was not significantly affected by preloading injection of indomethacin (5–10 mg/kg) to depress prostaglandin synthesis. Consistent with studies by others, a rise in filtration fraction was observed in 4 of 5 experiments with indomethacin but not in its absence. The results do not support the concept that the hypothetical natriuretic hormone is a Pg or is dependent upon a Pg for its synthesis or release. The data, moreover, constitute further evidence that the nutriuresis of acute volume expansion does not depend upon decreased colloid osmotic pressure in the renal peritubular capillaries. Urinary Pg F_2αexcretion was depressed by indomethacin but was unaffected by expansion. Expansion was associated with an unexplained 10 percent decrease in plasma potassium concentration.