292 Z. Fejfar 



effect more than ammoniuin chloride and simultaneously 

 compensated the potential loss of potassium. As the loss of 

 potassium from the cells is probably connected with a break- 

 down of cellular glycogen and protein, it is advantageous to 

 add N hormones (methylandrostendiol) to the treatment. 



It is not easy to correct completely a severe potassium 

 deficiency in chronic congestive failure. Even with a high 

 potassium intake it may be several weeks before cells become 

 saturated (Cort and Matthews, 1954). 



There remain many unanswered questions. It is customary 

 to treat patients with congestive failure with a low sodium 

 diet. It has been shown, however, that a low sodium diet in 

 healthy subjects increases aldosterone excretion in the urine 

 (Luetscher and Axelrad, 1954; Liddle, Duncan and Bartter, 

 1956; Wolff et at., 1956a, h), while a diet rich in sodium has 

 led to a decrease of aldosterone activity in the urine (Luet- 

 scher and Curtis, 1955a, h\ Gordon, 1955; Bartter et al., 1956; 

 Garrod, Simpson and Tait, 1956). 



Potassium administration also increases the excretion of 

 aldosterone (Laragh and Stoerk, 1955; Luetscher and Curtis, 

 1955a, b; Falbriard et ah, 1955; Bartter et al, 1956). 



Laragh and Stoerk (1957) recently demonstrated that no 

 sodium-retaining activity was found in the urinary extracts 

 from dogs on a diet low in both sodium and potassium. When 

 the amount of potassium was increased, hyperkalaemia 

 developed and sodium-retaining activity appeared in the urine. 

 Similar results were observed in one patient suffering from 

 rheumatic heart disease with congestive failure. As long as he 

 was kept on a diet low in sodium (about 12 m-equiv. daily) 

 and a rather high potassium intake (140 m-equiv.), the 

 excretion of aldosterone was high (about 300 (JLg./24 hr.). 

 After the marked reduction of serum potassium to 2*7 

 m-equiv. by an injection of 2 ml. of Mercuhydrine together 

 with a low potassium diet, the excretion of aldosterone fell 

 to 35 [jLg. Restoration of a normal serum potassium level by 

 administration of potassium was again followed by a very 

 marked excretion of aldosterone in the urine (630 (xg./24 hr.). 



