Calcium-Induced Potassium Transport in Cell Membranes

Abstract

Studies in the 1930–1940s, directed toward the elucidation of the connection between cell metabolism and ion—water content of human red cells, noted extreme alterations in K⁺ leakage under various experimental conditions. In lead-poisoned red cells (Ørskov, 1935), and in NaF-treated cells, Wilbrandt (1937, 1940) observed an increase in net K⁺ efflux and a concomitant cell shrinkage. It was first demonstrated by Gárdos (1956, 1958a,b, 1959) that, in metabolically depleted red cells, the enhanced K⁺ efflux took place only when Ca²⁺ ions were present in the suspending media. Since that time, it has been firmly established that rapid K⁺ transport in red cells is triggered by a specific interaction of Ca²⁺ ions with the intracellular membrane surface (see Section II-B), and the process, often noted in the literature as the “Gárdos phenomenon,” has become a model system to entertain numerous membrane physiologists, biochemists, and biophysicists. Training courses in membrane biology use this easily reproducible phenomenon to illustrate specificity, side-dependent activation, and selectivity of natural transport processes. Established research workers, deeply involved in the investigation of complex phenomena in complex cellular systems, from time to time return to the red-cell Ca²⁺ -induced K⁺ transport* to reveal new and important aspects of this process. The Ca²⁺ -induced K⁺ transport in red cells gave new insights into the coupling of ion movements to changes in membrane potential, and into the problem of side-dependent triggering and gating of ionic channels. In the meantime, as it generally occurs with red cell membrane phenomena, the phenomenon has turned out to be present in many animal cell membranes.