It is known that aldosterone, an 18-aldocorticosterone produced by the adrenal cortex, stimulates the sodium-for-hydrogen and the sodium-for-potassium exchange in the cells of the distal tubulus of the kidney. By increasing or decreasing the rate of tubular sodium reabsorption and thereby controlling the sodium content of the body, the varying levels of circulating aldosterone represent an important factor in homeostatic regulation of fluid volume. Increased urinary excretion of aldosterone-like sodium retaining material was shown by several investigators in patients with liver cirrhosis with ascites (Axelrad et al., 1955; Chart & Shipley, 1953; Luetscher & Johnson, 1954; Perry & Fyles, 1953; Duncan et al., 1956; Wolff & Koczorek, 1955). These findings support the view that the increased sodium conserving activity of the adrenal cortex may be involved in the formation of hydropic disease. It is also known that adiuretin, an octapeptide-hormone secreted by the neurohypophysis, activates the facultative reabsorption of water
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Wolff et al. (1958) studied this question.