Kaliuretic Response to Aldosterone: Influence of the Content of Potassium in the Diet

The excretion of potassium (K⁺) decreased by 50% (30 v 63 mEq/d, P < .01) when subjects consumed a diet that was low in K⁺ for 3 days. Although part of this conservation of K⁺ was achieved in part by suppressing the release of aldosterone, nevertheless providing exogenous mineralocorticoids did not lead to a large kaliuresis when there was a modest degree of K⁺ depletion. Accordingly, the purpose of this study was to evaluate possible mechanisms for this antikaliuretic response to mineralocorticoids. The renal handling of K⁺ was examined by independent analysis of the two factors that influence its excretion, the driving force to secrete K⁺ and the urine volume. This driving force is reflected in a noninvasive fashion by the transtubular [K⁺] gradient (TTKG). Stimuli to increase the rate of excretion of K⁺ in subjects on a normal and a low-K⁺ diet included the administration of 200 δg fludrocortisone (9αF), the induction of a high urine flow rate (9αF + furosemide), the induction of bicarbonaturia (9αF + acetazolamide), and the excretion of Cl^--poor urine (<15 mEq/L). On the low-K⁺ diet, the peak value for the TTKG 3 to 4 hours after 9αF was less than half that while on the normal diet (6.4 v 14, P < 0.01). In contrast, the TTKG was not significantly different on either diet when there was bicarbonaturia or the excretion of a Cl^--poor urine (18 v 17 and 17 v 16, respectively). The maximum rate of excretion of K⁺ during high volume diuresis on the low-K⁺ diet was not significantly different from that on a normal-K⁺ diet (193 and 211 δmol/min; flow, 9.2 and 8.3 mL/min, respectively). Of special importance, unlike the results on the normal diet, there was not a significant decline in the TTKG when the urine flow rate increased 10-fold while subjects consumed the low-K⁺ diet, at which time the TTKG was similar to that on the normal diet (5.8 v 6.6, respectively). Thus, the low net secretion of K⁺ in the cortical collecting duct (CCD) on the low-K⁺ diet was independent of mineralocorticoid levels and was only expressed at low rates of urine flow and in the absence of bicarbonaturia.