Response of the renal K+-conserving mechanism to kaliuretic stimuli: evidence for a direct kaliuretic effect by furosemide.

Isolated perfused kidneys from rats given a K+-free diet for 3 days demonstrate striking renal K+ conservation by a mechanism that is independent of perfusate and renal tissue K+, aldosterone, urine pH, urine flow, and sodium and anion excretion. To examine the effect of several kaliuretic stimuli on this intrinsic renal K+-conserving mechanism, kidneys from K+-depleted rats perfused with 3.5 mmol/L K+ were subjected to an experimental maneuver after 45 minutes of perfusion under normal conditions. Fractional potassium excretion (FEK) remained stable in time controls during a subsequent 45 minutes of perfusion. Acidification of the perfusate to pH 6.96 by addition of HCI had no significant effect on FEK. Alkalinization to pH 7.7 by either addition of NaHCO3 or a reduction in PCO2 resulted in significant kaliuresis (FEK 26% vs. 15%), which appeared to be a direct result of systemic alkalinization. Addition of Na2SO4 to the perfusate also produced significant kaliuresis (FEK 29%), which could not be dissociated from the magnitude of the natriuresis. Although both alkalosis and sulfate increased K+ excretion by depleted kidneys, FEK was much lower than with kidneys from normal rats perfused at pH 7.4 (FEK 51%). Thus the intrinsic renal K+-conserving mechanism dramatically diminishes the kidneys' kaliuretic potency and probably accounts for the blunted kaliuretic effect of these stimuli during K+ depletion in vivo. An increase in sodium excretion and urine flow rate achieved by lowering the perfusate albumin concentration, increasing the perfusate pressure, or adding the diuretics hydrochlorothiazide and furosemide resulted in significant kaliuresis.(ABSTRACT TRUNCATED AT 250 WORDS)