RESUMO
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 ( approximately 37%), sulfate ( approximately 32%), or bicarbonate ( approximately 62%), and also when the pH of the control perfusate was increased ( approximately 26%). The majority (80%) of acetate-stimulated J(K) was Ba(2+) sensitive, but furosemide (1 mM) further reduced secretion ( approximately 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 Ba(2+), 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.