Abstract
To determine the specific effects on renal potassium transport of acute elevations in plasma aldosterone, dexamethasone, and potassium concentrations, we studied adrenalectomized rats prepared such that each factor could be varied independently. Clearance data alone could not be used to deduce the underlying tubular transport effects, however, since infusion of each of these agents was associated with a marked change in urinary flow rate, which may itself have influenced potassium excretion. We therefore used a technique of continuous microperfusion, in vivo, of single superficial distal tubules to evaluate potassium secretion at constant luminal flow rate during each experimental maneuver. Acute aldosterone infusion was associated with a 90% stimulation of potassium secretion by microperfused tubules. However, total kidney sodium excretion and urinary flow rate were markedly reduced, and these factors opposed the direct tubular action of aldosterone, resulting in no net change in the amount of potassium excreted into the final urine. Conversely, dexamethasone had no direct effect on potassium secretion by single microperfused tubules, but it caused a sharp increase in urinary flow and sodium excretion, and secondarily enhanced urinary potassium excretion by 50%. Hyperkalemia per se stimulated renal potassium excretion both via a direct tubular effect and by increasing urinary flow rate. We conclude that urinary potassium excretion after infusion of each of these agents represents the net result of direct tubular effects and secondary flow-mediated changes.