60 Discussion 



We have made an observation on animals that is not identical but 

 may point in the same direction as the observation you have made. If 

 adrenalectomized rats are given a very high salt load, hypernatraemia is 

 produced in a relatively short time. Firstly, then, the sensitivity to ADH 

 and pitressin decreases considerably. We did not get any serum values 

 but in the urine there is a strong dilution due to the greater urinary out- 

 put. Secondly, treatment with aldosterone in relatively high doses for 

 four or five days causes sensitivity to pitressin to disappear completely. 



Fourmcm : With high aldosterone dosage there is certainly an expansion 

 of the extracellular fluid, and it may be that this expansion diminishes 

 the sensitivity to pitressin. 



As regards the steroid assays, I do know that Schwartz and Bartter's 

 cases, which were analogous in many ways, were not salt-deficient; they 

 had an expanded extracellular volume and the aldosterone output in the 

 urine was normal. A. Gowenlock in Manchester measured the aldo- 

 sterone output in one of our patients and it was normal. We also did 

 17-ketosteroid assays as a crude measure of their corticoid output, and 

 the results were normal. It is obvious that the hyponatraemia does not 

 lead to a stimulation of the aldosterone output of the adrenal. 



Desaulles : Could this be given the same interpretation as the findings 

 of Prader, Spahr and Neher (1955. Schweiz. rued. Wschr., 85, 1085)? 

 There may be some form of sodium-losing syndrome. 



Adolph : It seems to me. Dr. Fourman, that in order to show that there 

 is something more to one of these syndromes than a lack of drinking 

 behaviour or drinking response on the part of the individual, you have to 

 perform your tests in a certain order ; you have to be sure that the patient 

 has plenty of water when you do the salt test and plenty of salt when you 

 do the water test. Could you have switched the tests around and still 

 obtained the same results? 



Fourman : The saline load was done three weeks before the dehydra- 

 tion. The dehydration preceded the pitressin by one day in one of the 

 patients, by a week in the other patient. The pitressin test was accom- 

 panied by a load of water at the time. I do agree that one test can 

 influence another but I do not think that they did in this instance. 



Borst : When a high or a low sodium concentration in the blood plasma 

 is maintained we believe that this is almost always due to an insuf- 

 ficient circulation. This insufficiency often results from dehydration, but 

 it may have other causes such as cardiac failure or hypoproteinaemia. 

 We found a high blood sodium in anaemic patients who had had 

 recurrent haemorrhages from peptic ulcer. They had no free access to 

 water and had been treated with abundant saline infusions; they had 

 substantial oedema. During several days the urine contained less 

 sodium than tap water, After a large transfusion of blood the sodium 

 excretion started and the blood sodium fell to a normal level. Simul- 

 taneously, the output of water increased and the urea concentration of 

 the urine, which had been very high, decreased. The counterpart was 

 observed in cachectic patients with anaemia and hypalbuminaemia who 

 adhered to a salt-free diet and who had a liberal intake of water. They 

 maintained a low blood sodium concentration in the presence of oedema. 



