Hormones and Water and Electrolyte Metabolism 89 



quantity during pregnancy has been shown by numerous 

 balance studies (see Rinsler and Rigby, 1957 for references). 

 Chesley and Boog (1943) found an increased thiocyanate 

 space in normal pregnancy, the increase being still greater 

 in pre-eclamptic toxaemia. From this it was concluded that 

 much of the sodium retention was due to expansion of the 

 extracellular fluid (ECF) compartment. However, Gray and 

 Plentl (1954), using a sodium isotope dilution technique, 

 found little change in the sodium space and total exchange- 

 able sodium in normal pregnancy. They observed a total gain 

 of some 500 m-equiv. of sodium during the last six months of 

 pregnancy, which they felt could be accounted for by the 

 products of gestation and the expanded maternal blood 

 volume. The maintenance of an essentially unchanged non- 

 pregnant sodium space during normal pregnancy, despite the 

 rise in plasma volume, suggests that there is little change in 

 ECF. 



The gain of sodium and water, with maintenance of a 

 normal total-exchangeable sodium value and with an in- 

 creased thiocyanate space, provides indirect evidence that in 

 normal pregnancy there is an alteration of cell permeability 

 with an increased maternal storage of intracellular sodium and 

 water. The increased intracellular storage of sodium, together 

 with the foetal requirements, are a drain on the salt content 

 of the ECF, which, if uncorrected, would lead to diminution 

 of the ECF and plasma volumes. It has been demonstrated 

 by Bartter and co-workers (1956) that a fall in ECF volume 

 without change in tonicity leads to a rise in aldosterone 

 excretion. Such a rise in aldosterone excretion occurs in 

 pregnancy (Venning and Dyrenfurth, 1956; Venning et al., 

 1957; Rinsler and Rigby, 1957) and may form part of a 

 homeostatic mechanism for maintaining the ECF volume and 

 meeting the loss of sodium from the ECF into the maternal 

 cells and foetal tissues by increased renal reabsorption. 



In pre-eclamptic toxaemia, clinical examination alone is 

 sufficient to demonstrate the expanded ECF compartment. 

 Expansion of this compartment was shown by Bartter and 



