Activation of luminal Na+/H+ exchange in distal nephron of frog kidney. An early response to aldosterone.

Increased chronic intake of K+ induces H+ and K+ secretion in amphibian distal tubule, paralleled by an elevation of plasma aldosterone. The present experiments test whether the mineralocorticoid hormone is responsible for the alteration of ion transport. The blood capillaries of the isolated kidneys of NaCl-adapted (i.e. aldosterone-suppressed) Rana pipiens were perfused with HEPES-buffered amphibian Ringer solution (pH 7.8). Limiting intraluminal pH (pHlu) was measured continuously with pH-sensitive microelectrodes while aldosterone (3 X 10(-7) to 3 X 10(-6) mol/l) was applied in the peritubular perfusate. Concomitant with a decrease of the lumen-positive transepithelial potential (Vte) from 8.5 +/- 1.1 mV to 4.0 +/- 0.6 mV pHlu dropped from 7.73 +/- 0.02 to a new steady-state value of 7.17 +/- 0.05 within 60 to 180 min of aldosterone administration. Significant luminal acidification occurred already 20 min after application of aldosterone. Luminal addition of 10(-3) mol/l amiloride reversed luminal acidification to a pHlu of 7.68 +/- 0.04; at the same time Vte recovered partially. Pretreatment of the distal tubules with spironolactone prevented the aldosterone-induced acidification of the tubule fluid. We conclude that in early distal tubule of the amphibian kidney aldosterone--after interaction with cytoplasmic receptors--activates the luminal, amiloride-inhibitable Na+/H+ exchanger. This mechanism could explain enhanced H+ secretion found in the K+ adapted animal.