Water and Electrolytes in Congestive Failure 279 



Bucht and co-workers (1953) studied the haemodynamic 

 changes together with the excretion of sodium in eight healthy 

 human subjects during muscular exercise of varying degree. 

 As long as the effort was small (oxygen consumption not 

 above 500 ml./niin.), an increase of CO was found without 

 significant effect on renal blood flow, glomerular filtration 

 rate or excretion of sodium. A greater muscular effort 

 (oxygen consumption about 1,000 ml./min.) was character- 

 ized by a marked increase in CO (almost double) and a 

 simultaneous fall in renal blood flow and the renal fraction of 

 CO. The excretion of sodium and water fell. Glomerular 

 filtration rate and pressure in renal veins did not change 

 significantly. Similar results were observed in patients with 

 heart disease (Judson et al., 1955; Himbert, Scebat and 

 Theard, 1956). Increase of tubular reabsorption was there- 

 fore responsible for the diminished excretion of sodium and 

 water. 



The close relationship between renal blood flow and excre- 

 tion of electrolytes in congestive failure is striking. We have 

 expressed the opinion (Brod and Fejfar, 1950) that decreased 

 renal blood flow directly impairs the excretion of water and 

 electrolytes. A smaller glomerular filtration rate diminishes 

 tubular electrolyte load and, owing to a slower flow of tubular 

 urine, a greater proportion of the filtered amount is reabsorbed. 

 We could not, of course, exclude another possibility: that 

 increased reabsorption of water and electrolytes in the renal 

 tubules could occur parallel with, but independently of the 

 diminished renal plasma flow; i.e. the stimulus for the renal 

 vasoconstriction could directly influence the function of renal 

 tubules, leading to an increased reabsorption of salt and water. 



Humoral and neural regulatory mechanisms in 

 congestive failure. 



Some known humoral and neural factors can alter the 

 function of renal tubules. In the urine of patients with con- 

 gestive failure renin (Merrifl, Morrison and Brannon, 1946), 

 VEM (vaso-excitor material) and VDM (vasodepressor 



