THE CONCENTRATION EFFECT WITH VALONIA: POTENTIAL DIFFERENCES WITH DILUTED POTASSIUM-RICH SEA WATERS.
The concentration effect with sea waters containing more than the normal amount of potassium has been studied in Valonia macrophysa. This was done by comparing the initial changes in P.D. across the protoplasm when natural sea water bathing the cell was replaced by various isotonic dilutions of KCl-rich sea waters. With small dilutions of KCl-rich sea waters, the P.D.-time curves are of the same form as with the undiluted solution, exhibiting the fluctuations characteristic of KCl-rich solutions. This indicates that with these solutions K(+) enters Valonia protoplasm and plays an important part in the P.D. The value of the initial rise in P.D. decreases with increasing dilution. With high dilutions of KCl-rich sea waters, the P.D.-time curves are of quite different shape, resembling the curves with diluted natural sea water; the P.D. is practically independent of small changes in the concentration of potassium, and increases with increasing dilution. That is, with these higher dilutions, the sign of the concentration effect is reversed, becoming the same as with diluted natural sea water. The greater the concentration of KCl in the undiluted sea water, the higher is the critical dilution at which K(+) ceases to influence the P.D. For a wide range of sea waters containing both KCl and NaCl, it is shown that the concentration effect above the critical dilution is determined solely by the activity of NaCl in the external solution. It is concluded that with dilute natural sea water and with high dilutions of KCl-rich sea waters we have to do with a diffusion potential, involving only the Na(+) and Cl(-) ions, which are diffusing out from the vacuole. A quantitative relation between the composition of the sea water and the critical dilution has been deduced from the classical theory of the diffusion of electrolytes. It is shown that with dilutions less than this critical value the diffusion of K(+) in the outer non-aqueous layer of the protoplasm is directed inward; hence K(+) enters the protoplasm from these solutions. With dilutions greater than the critical value, the diffusion of K(+) in this layer is directed outward; hence K(+) does not enter the protoplasm. Since the P.D. shows no evidence of this outward diffusion of K(+), it is concluded that the amount of K(+) ordinarily present in the protoplasm is too small to produce any lasting electrical effect, and that the outward diffusion of K(+) from the vacuole is prevented by the mechanism responsible for the accumulation of KCl in the cell sap.
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Laboratories of The Rockefeller Institute for Medical Research.