Role of luminal anion and pH in distal tubule potassium secretion

Abstract

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 (∼37%), sulfate (∼32%), or bicarbonate (∼62%), and also when the pH of the control perfusate was increased (∼26%). The majority (80%) of acetate-stimulated J K was Ba2+sensitive, but furosemide (1 mM) further reduced secretion (∼10% 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.