This preclinical study characterizes the kinetics of potassium exchange in cat ventricular muscle, demonstrating its dependence on external potassium concentration and sensitivity to ouabain.
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Informs models of digitalis effects on myocardial K balance; leaves open translation to human arrhythmia or hyperkalemia management.
The exchange of cell K with K(42), J(K), has been measured in cat right ventricular papillary muscle under conditions of a steady state with respect to intracellular K concentration. Within the limits of the measurement, all of cell K exchanged at a single rate. Cells from small cats are smaller and have larger surface/volume ratios than cells from large cats. The larger surface/volume ratio results in larger flux values. J(K) increases in an approximately linear manner as the external K concentration is increased twentyfold, from 2.5 to 50 mM, at constant intracellular K concentration. The permeability for K ions, P(K), calculated from the influx and membrane potential, remains very nearly constant over this range of external K concentrations. J(K) is not affected by replacement of O(2) by N(2), or by stimulated contractions at 60 per minute, but K influx decreases markedly in 10(-5)M and 10(-8)M ouabain.
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Goerke et al. (1965) studied this question.
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