Solid state theory of competitive diffusion of associated Na+ and K+ in cells by free cation and vacancy (hole) mechanisms, with application to nerve.
If, as recent evidence indicates, most cell potassium is associated with macromolecular fixed charge, then diffusion of potassium ions in cells might occur by (1) diffusion of the small fraction of free potassium in cell water (analogous to electrons in the conduction band of a semiconductor) or by (2) diffusion of vacancies on association sites (analogous to holes in a semiconductor). Derivations of the Fick first law of diffusion predict that partial substitution of sodium for potassium in the cell produces opposite effects on the effective diffusion constant of potassium for those mechanisms. Application of that substitution to nerve data suggests that rubidium ions diffuse by a free cation result when the nerve is clamped at its resting potential, but by a vacancy mechanism when the nerve is clamped at zero voltage.
D002414:Cations, Monovalent; D002477:Cells / Q000378:metabolism*; D004058:Diffusion; D004558:Electric Stimulation; D046911:Macromolecular Substances; D008954:Models, Biological; D009417:Nerve Tissue / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*
D002414:Cations, Monovalent; D046911:Macromolecular Substances; D012964:Sodium; D011188:Potassium