234 ELECTROLYTES IN BIOLOGICAL SYSTEMS 



apparatus). This mechanism opposes the exchange of potassium in the surface 

 (so-called intracellular potassium) for extracellular sodium. Such ion exchange 

 does occur under certain conditions, e.g., when extracellular potassium is low. 

 This situation, as has been pointed out, leads to diminished net salt transport 

 across the skin. In the 'adsorption-desorption pump', metabolic reactions may 

 act upon potassium or upon sodium or upon both ions. 



2) A redox pump, of the kind described by Conway, is visualized which is 

 designed to carry sodium ions across a boundary between epidermis and corium, 

 a boundary that the free ion could not pass. If the site of the redox pump in 

 the epidermis is nearer the basal part of the epithelial cells, it is not difficult 

 to see that the redox pump could become dependent on the supply of sodium. 

 This, however, is regulated by the 'adsorption-desorption pump', which is pro- 

 posed to precede the redox pump. 



In the light of this hypothesis, some of the disturbances in active salt trans- 

 port in isolated frog skin may be interpreted as follows: cyanide abolishes active 

 salt transport because it blocks, directly, the redox pump and also, indirectly ,^ 

 the adsorption-desorption pump. Low potassium ion concentration of the en- 

 vironment drastically diminishes active salt transport because it leads to 

 Kt^Na^ exchange and, hence, to trapping of sodium in the cell surfaces. 

 Entrance of sodium into the skin from the outside may become more difficult. 

 In such an event, sodium would not reach the redox pump which normally 

 carries sodium across the skin. As a result of insufficient supply of sodium to the 

 redox pump, net salt transport becomes smaller. Because of a spatial separation 

 of the two metabolic processes in which sodium is supposedly involved, dinitro- 

 phenol, by uncoupling oxidation from phosphorylation, would also lead to 

 uncoupling of oxidation from active sodium transport. The sodium carrier of 

 the redox pump would then be relieved of its double burden of keeping the 

 mechanism of oxidation going and, at the same time, of pulling sodium along. 

 It is not difficult, then, to understand why dinitrophenol leads to inhibition of 

 active salt transport in frog skin, while oxidation proceeds at a higher than 

 normal rate. 



Trapping of sodium ions, resulting from K| <=^ Na^ exchange, means, in 

 electrical terms, increase of sodium resistance and decrease of sodium current. 

 This is in agreement with data presented by Ussing (76) and by Fuhrman (9). 

 In K+-free Ringer's, the short circuit current dropped from about 44 to 4 /xamp 

 cm~^. Dinitrophenol increased sodium resistance of skin, especially if the initial 

 resistance was low. It was found, e.g. that application of 0.05 mM/l.of dinitro- 

 phenol raised the resistance from about 2000 to 6000 S2 cm~''. It remains to be 

 seen whether dinitrophenol induces K^ ^ Na^ ion exchange. This is likely 

 since Levinsky and Sawyer (44) have found that treatment of skin with dinitro- 

 phenol leads to loss of skin potassium. 



