Failure to demonstrate non-aldosterone salt-retaining substances in plasma, urine, and liver extract of chronic caval dogs.

Abstract

The combined factors of depressed renal function and hyperaldosteronism by themselves do not adequately explain the progressive sodium retention of the chronic caval dog. The possibility that non-aldosterone salt-retaining humoral factors may play a major role in the sodium retention of this edema state has not previously been explored using bioassay techniques. In the present study we obtained ascitic fluid and plasmas from a variety of drainage areas from both control and caval dogs and infused them directly into the left renal artery of small dogs, pretreated with large doses of DOCA and undergoing a modest natriuresis. No decrement in sodium excretion was observed. When arterial plasma, hepatic venous plasma, ascitic fluid, urine, and saline extracts of liver were fractionated and concentrated up to 200 times, no evidence for a non-aldosterone antinatriuretic factor could be obtained in the bioassay system for fractions in the range 500 – 50 000 molecular weight. Within the limitations of the preparative and bioassay techniques used, we could therefore not obtain any evidence for the existence of non-aldosterone salt-retaining substances in the plasma, urine, or liver of chronic caval dogs.