300 Discussion 



intracellular water or total intracellular potassium. This is a change 

 which may also be seen in severe weight loss without congestive failure, 

 and the situation is very difficult to evaluate because patients with con- 

 gestive failure will often have lost weight in the late stages. An inter- 

 esting finding was that although there were almost equal degrees of 

 congestive failure the average intracellular potassium concentration ap- 

 peared normal in the males but was low in the females. We have no 

 explanation for this finding. 



The question to us, however, is whether a low average intracellular 

 potassium concentration means a reduction in the relative amount of 

 potassium or too much water in the cells. We cannot answer this. In 

 tissue analysis results we are faced with the same question : when there 

 is a low intracellular potassium concentration related to the intracellular 

 water, is there too little potassium or too much water? The relationship 

 of potassium to nitrogen or phosphorus does not seem to change very 

 much. This might suggest that it is as much an increase in water as it is a 

 decrease of potassium in the cells. 



There are conflicting opinions on the balance studies. Most American 

 studies demonstrate a positive potassium balance during recovery from 

 congestive failure. However, most of these studies have been carried out 

 on low sodium/high potassium intake, and the high potassium intake may 

 explain the positive potassium balance. In a study made in Switzerland 

 a medium-sized intake of potassium was used and no positive potassium 

 balance during recovery from congestive failure was seen. 



Milne : There seem to me to be two sides to this question of assessing 

 the cause of secondary aldosteronism in relation to the expansion and 

 contraction of body fluids. There is the physiological stimulus in haemor- 

 rhage, shock, etc., where, as you say, there is contraction ; and there is the 

 pathological stimulus in the nephrotic syndrome, cardiac failure, and 

 hepatic cirrhosis, where there is expansion. All this is really tied up with 

 the philosophy of volume receptors. It always seems to me to be im- 

 possible for the body to have a true volume receptor. The only way we 

 know of measuring volume is to pour fluid into a graduated cylinder. I 

 feel the only possible explanation is that the body is relating tension to 

 volume, and that the receptors are tension receptors for either static or 

 pulsatile tension. I think the stimulus is the same in all forms of secon- 

 dary aldosteronism and that the receptors must be on the arterial side of 

 the circulation. 



Fejfar: I agree with you about volume and stretch receptors. I would 

 like to add that if one gives sodium to patients with congestive failure, the 

 aldosterone excretion decreases (Gordon, 1955); these people therefore 

 react in the same way as normal persons, although their actual levels of 

 aldosterone may be higher. 



