1. Recent investigation has shown that sodium excretion is greater following portal venous infusion of 5% sodium chloride (w/v) than after systemic infusion in anaesthetized dogs. It was suggested that a factor of hepatic origin which is capable of depressing renal tubular reabsorption may be involved in this response. The present experiments were undertaken to determine the renal responses of conscious, unanaesthetized dogs to infusions of 5% NaCl administered systemically and by the portal venous routes.
2. No differences were observed in urine flow or sodium excretion rates in normal dogs when responses to the two routes of NaCl infusion were compared; potassium excretion was elevated following systemic as compared to portal NaCl infusion (P < 0·05). Urine flow was significantly greater (P < 0·05) in vasopressin and mineralocorticoid treated dogs following portal infusion of 5% NaCl, but no differences in electrolyte excretion were observed between routes of administration.
3. These findings are not compatible with the concept that a natriuretic factor is released from the liver consequent to elevation of portal venous sodium concentration in the conscious dog.