Role of luminal anion and pH in distal tubule potassium secretion

Potassium secretory flux (J(K)) by the distal nephron is regulated by systemic and luminal factors. In the present investigation, J(K) was measured with a double-barreled K+ electrode during paired microperfusion of superficial segments of the rat distal nephron. We used control solutions (100 mM NaCl, pH 7.0) and experimental solutions in which Cl- had been replaced with a less permeant anion and/or pH had been increased to 8.0. J(K) increased when Cl- was replaced by either acetate (similar to37%), sulfate (similar to32%), or bicarbonate (similar to62%), and also when the pH of the control perfusate was increased (similar to26%). The majority (80%) of acetate-stimulated J(K) was Ba2+ sensitive, but furosemide (1 mM) further reduced secretion (similar to10% of total), suggesting that K+-Cl- cotransport was operative. Progressive reduction in luminal Cl- concentration from 100 to 20 to 2 mM caused increments in J(K) that were abolished by inhibitors of K+-Cl- cortransport, i.e., furosemide and [( dihydroindenyl) oxy] alkanoic acid. Increasing the pH of the luminal perfusion fluid also increased J(K) even in the presence of Ba2+, suggesting that this effect cannot be accounted for only by K+ channel modulation of K+ secretion in the distal nephron of the rat. Collectively, these data suggest a role for K+-Cl- cotransport in distal nephron K+ secretion.