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Extrarenal potassium transport and the beta 2-adrenergic system.

The distribution of a short-term potassium load was quantitated in three groups of acutely nephrectomized rats infused with KCl at 0.75, 1.50, and 2.25 mEq/kg/hr for 90 minutes. The rate of net potassium transfer from the extracellular fluid compartment to the intracellular fluid compartment was stable from 30 to 90 minutes and proportional to the rate of infusion, with no evidence of saturation of transport mechanisms. In the period 60 to 90 minutes, the calculated increments in intracellular potassium concentration over 10-minute intervals were similar to the respective increments in extracellular potassium concentration. The apparent volume of distribution of the infused potassium over this period was similar to total body water. At the termination of the infusions, the net potassium transfer rates rapidly fell to very low levels. Our studies support the view that the extrarenal modulation of short-term potassium load is dependent on changes in plasma potassium concentration that conform to a first-order linear kinetic model. The infusion of the selective beta 2-adrenergic blocker butoxamine without potassium administration to acutely nephrectomized rats resulted in a net efflux of potassium from the intracellular fluid compartment. The addition of butoxamine to three groups of rats receiving KCl at the previous rates resulted in a fixed decrement in net potassium transfer to the intracellular fluid compartment that was not significantly different from the net efflux of potassium seen with butoxamine alone. Despite beta blockade, the net transfer of potassium remained proportional to the infusion rate. Thus, in our studies, beta 2-adrenergic blockade had a relatively fixed influence on decreasing net potassium transfer, both under basal conditions and during short-term potassium administration.