title: 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 ( 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.
authors.affiliation: Basic Science Department, Faculdade de Odontologia de São José dos Campos, Instituto de Ciências Biomédicas, Universidade de São Paulo, 05508-900 São Paulo, Brazil.
authors.forename: J B O
authors.initials: JB
authors.lastname: Amorim
authors.forename: M A
authors.initials: MA
authors.lastname: Bailey
authors.forename: R
authors.initials: R
authors.lastname: Musa-Aziz
authors.forename: G
authors.initials: G
authors.lastname: Giebisch
authors.forename: G
authors.initials: G
authors.lastname: Malnic
mesh_terms: D000085:Acetates / Q000494:pharmacology; D000818:Animals; D000838:Anions / Q000378:metabolism* / Q000494:pharmacology; D001464:Barium / Q000494:pharmacology; D001639:Bicarbonates / Q000494:pharmacology; D006859:Hydrogen / Q000502:physiology*; D006863:Hydrogen-Ion Concentration; D007686:Kidney Tubules, Distal / Q000378:metabolism*; D008297:Male; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D013431:Sulfates / Q000494:pharmacology; D027981:Symporters / Q000502:physiology; D000096922:K Cl- Cotransporters
chemical_list: D000085:Acetates; D000838:Anions; D001464:Barium; D001639:Bicarbonates; D006859:Hydrogen; D011188:Potassium; D013431:Sulfates; D027981:Symporters; D000096922:K Cl- Cotransporters