title: Calcitonin activates an Na(+)-independent HCO3(-)-dependent pathway in the rabbit distal convoluted tubule.
abstract: Calcitonin is known to stimulate Ca2+ reabsorption and natriuresis and to increase adenosine 3',5'-cyclic monophosphate levels in early distal tubule, but its effects on acid-base transport mechanisms are not well characterized in this segment. We found that recovery of cell pH (pH1) from an induced acid load (using NH4+) in single isolated segments of the initial portion ("bright") of the rabbit distal convoluted tubule (DCTb) was due to an ethylisopropylamiloride-sensitive Na+/H+ exchanger both in the absence and presence of HCO3-, but we found no evidence for participation of other mechanisms such as an H+ pump or an HCO3(-)-dependent mechanism. Introduction of calcitonin stimulated an Na(+)-independent, HCO3(-)-dependent mechanism (0.17 +/- 0.04 pH units/min, n = 14) that reestablishes normal pHi after an induced acid load. This mechanism was observed only in the presence of CO2/HCO3- and was not inhibited by N-ethylmaleimide (1 mM), 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (200 microM), or Sch-28080 nor stimulated by glutamine (2 mM) or ketoglutarate (0.5 mM), but it was dependent on chloride. We conclude that, in the DCTb, salmon calcitonin activates a latent Na(+)-independent, HCO3(-)-dependent mechanism.
authors.affiliation: Laboratoire de Physiologie Cellulaire, Collége de France, Paris, France.
authors.forename: G
authors.initials: G
authors.lastname: Dagher
authors.forename: S R
authors.initials: SR
authors.lastname: Thomas
authors.forename: N
authors.initials: N
authors.lastname: Griffiths
authors.forename: S
authors.initials: S
authors.lastname: Siaume-Perez
authors.forename: C
authors.initials: C
authors.lastname: Sauterey
mesh_terms: D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / Q000494:pharmacology; D000584:Amiloride / Q000031:analogs & derivatives / Q000494:pharmacology; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism* / Q000494:pharmacology; D002116:Calcitonin / Q000494:pharmacology*; D002245:Carbon Dioxide / Q000494:pharmacology; D002712:Chlorides / Q000494:pharmacology; D000242:Cyclic AMP / Q000502:physiology; D005033:Ethylmaleimide / Q000494:pharmacology; D005973:Glutamine / Q000494:pharmacology; D006706:Homeostasis; D006863:Hydrogen-Ion Concentration; D007093:Imidazoles / Q000494:pharmacology; D066298:In Vitro Techniques; D007656:Ketoglutaric Acids / Q000494:pharmacology; D007686:Kidney Tubules, Distal / Q000187:drug effects / Q000502:physiology*; D008297:Male; D008856:Microscopy, Fluorescence; D000644:Quaternary Ammonium Compounds / Q000494:pharmacology; D011817:Rabbits; D012964:Sodium / Q000378:metabolism* / Q000494:pharmacology; D017923:Sodium-Hydrogen Exchangers / Q000378:metabolism
chemical_list: D001639:Bicarbonates; D002712:Chlorides; D007093:Imidazoles; D007656:Ketoglutaric Acids; D000644:Quaternary Ammonium Compounds; D017923:Sodium-Hydrogen Exchangers; C035235:Sch 28080; D005973:Glutamine; D002245:Carbon Dioxide; D000584:Amiloride; D002116:Calcitonin; D012964:Sodium; D000242:Cyclic AMP; D005033:Ethylmaleimide; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; C039614:ethylisopropylamiloride