280 Z. Fejfar 



material) have been found (Edelman et al., 1950). Extracts 

 of urine from patients with congestive failure contain anti- 

 diuretic materal (Bercu, Rokaw and Massie, 1949, 1950) with 

 a great sodium-retaining activity (Deming and Luetscher, 

 1950a,b), which disappears when the patients become com- 

 pensated (Luetscher, Deming and Johnson, 1950, 1951). 

 The substance responsible for this is aldosterone (Luetscher 

 and Johnson, 1954). An increased excretion of aldosterone is 

 not characteristic only of congestive failure, but accompanies 

 nephrotic and cirrhotic oedema as well. A permanent increase 

 of aldosterone under these conditions is called secondary 

 aldosteronism (Conn, 1955; Bartter, 1956; Milne and 

 Muehrcke, 1956; Thorn et a/., 1956; Liddle, Duncan and 

 Bartter, 1956; Wolff, Koczorek and Buchborn, 1957). 



The increased secretion of aldosterone in congestive failure 

 may be important in some patients, as can be seen from the 

 favourable effect of bilateral adrenalectomy (Thorn et al., 

 1956). 



Buchborn (1956) estimated the activity of plasma anti- 

 diuretic hormone (ADH) by a sensitive biological method on 

 the toad, together with serum osmolarity. He found a close 

 indirect correlation between the plasma ADH and serum 

 osmolarity in 14 normal subjects, in patients with hepatic 

 cirrhosis, in compensated cardiac patients, and also in patients 

 with congestive failure. The increased plasma level of ADH 

 in congestive failure is not therefore primary, being an ex- 

 pression of the homeostatic function of ADH, regulating 

 osmotic pressure in the organism (Buchborn, 1956). 



Neither ADH nor aldosterone significantly influences cir- 

 culation in the kidneys. Their main effect is on renal tubules, 

 where they increase the reabsorption of water (ADH), or 

 sodium (aldosterone). In addition we have already indicated 

 that the vasoconstriction in the kidneys, together with 

 diminished elimination of sodium, occurs during a short 

 muscular effort (10 minutes, Bucht et al, 1953). The effect of 

 aldosterone would be slower. According to Bartter (1956) the 

 excretion of sodium in a patient with Addison's disease did 



