Indirect Sodium-Retaining Action of Oxytocin on Dog Kidney

Summary

The action of synthetic oxytocin on renal sodium excretion was studied in dogs under barbiturate anesthesia given a moderate saline load. Left renal artery infusion of oxytocin at a rate 5 mU/kg per hour produced comparable and significant decreases in sodium excretion by the left and by the right kidney. Since reduction of oxytocin dose to 0.5—1.5 mU/kg per hour simultaneously abolished sodium retention by the infused and the contralateral kidney, it was concluded that oxytocin's action on the kidney was indirect. The observation that postoxytocin decrease in sodium excretion occurred with no significant changes in glomerular filtration rate suggested very strongly that the cause of sodium retention was an increase in renal tubular sodium reabsorption. These findings contradict most of the previous data which indicated saluresis and inhibition of tubular sodium transport by oxytocin, and suggest that oxytocin may have differential effects, depending on dosage and mode of administration. The mechanism of antinatriuretic action of oxytocin is unknown.