Stimulation of Na-K-ATPase in the rat collecting tubule by two diuretics: furosemide and amiloride.

To test whether sodium availability controls the concentration of renal Na-K-ATPase, we evaluated the effect of chronic alterations in apical membrane sodium permeability in specific nephron segments on the maximal activity of Na-K-ATPase. For this purpose Na-K-ATPase activity was determined in nephron segments microdissected from rats treated continuously for 3-8 days with either furosemide or amiloride, two diuretics known to lower the apical permeability to sodium in the thick ascending limb and the collecting tubule, respectively. Unexpectedly, Na-K-ATPase activity was decreased neither in the thick ascending limb nor in the collecting tubule after administration of either drug. In fact, both diuretics paradoxically increased the pump activity by 60-150% in the collecting tubule. This stimulation of Na-K-ATPase activity was accompanied with an enhancement of the collecting tubule diameter. Stimulation of Na-K-ATPase was identical in the collecting tubule of diuretic-treated rats receiving spironolactone. These results suggest that Na-K-ATPase maximal activity is not controlled by sodium availability or by aldosterone under these conditions and that chronic administration of furosemide or amiloride induces Na-K-ATPase activity in the collecting tubule. This effect appears to be independent of aldosterone.