title: Secondary hyperaldosteronism stimulates acidification in rat distal colon.
abstract: Recent studies from this laboratory have determined that colonic K+ absorption is altered by the PCO2 and by secondary hyperaldosteronism. Partial inhibition by vanadate and mucosal ouabain suggested the operation of an H+/K+ exchange pump. To determine the mechanism of acidification in rat distal colon, we measured in vitro acidification using the pH-stat technique by voltage-clamped segments of colonic epithelium in controls and in the presence of secondary hyperaldosteronism, induced by a sodium-deficient diet. Chronic stimulation with aldosterone resulted in increased mucosal acidification in vitro for at least 2 h. This effect could not be accounted for by lactate production and was not altered by elimination of the aldosterone-induced increase in voltage and short-circuit current with 10 microM amiloride. Studies with inhibitors and ion substitution revealed that mucosal acidification resulted from both Na-dependent and Na-independent mechanisms. Na-dependent acidification was inhibited by ATPase inhibitors and was mediated in part by a luminal Na+/H+ exchanger in the presence of secondary hyperaldosteronism. Na-independent acidification was mediated by a pathway dependent on luminal K+ that was inhibited by vanadate and mucosal ouabain, consistent with the operation of an H+/K+ exchange pump.
authors.affiliation: Department of Medicine, New England Medical Center, Tufts University School of Medicine, Boston, MA 02111.
authors.forename: M L
authors.initials: ML
authors.lastname: McLaughlin
authors.forename: D E
authors.initials: DE
authors.lastname: McBride
authors.forename: R D
authors.initials: RD
authors.lastname: Perrone
mesh_terms: D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D002352:Carrier Proteins / Q000502:physiology; D003106:Colon / Q000378:metabolism / Q000503:physiopathology* / Q000648:ultrastructure; D004032:Diet / Q000009:adverse effects; D004558:Electric Stimulation; D006859:Hydrogen / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D006929:Hyperaldosteronism / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D010042:Ouabain / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000172:deficiency / Q000502:physiology; D017923:Sodium-Hydrogen Exchangers; D014638:Vanadates / Q000494:pharmacology
chemical_list: D002352:Carrier Proteins; D007773:Lactates; D017923:Sodium-Hydrogen Exchangers; D019344:Lactic Acid; D014638:Vanadates; D010042:Ouabain; D000584:Amiloride; D006859:Hydrogen; D012964:Sodium; D000251:Adenosine Triphosphatases