Intestinal HCO3- secretion in Amphiuma: stimulation by mucosal Cl- and serosal Na+.
The requirement for Na+ and Cl- in the bathing media to obtain a maximal HCO3- secretory flux (JHCO3-) across isolated short-circuited Amphiuma duodenum was investigated using titration techniques and ion substitution. Upon substitution of media Na+ with choline, HCO3- secretion was markedly reduced. Replacement of media Cl- produced a smaller reduction of JHCO3-. The presence of Cl- enhanced HCO3- secretion only if Na+ was also in the media. Elevation of media Na+ or Cl- in the presence of the other ion produced a saturable increase of JHCO3-. In the presence of Na+, Cl- stimulated JHCO3- when added to the mucosal but not the serosal medium. In the presence of Cl-, Na+ elevated JHCO3- when added to the serosal but not the mucosal medium. The ability of mucosal Cl- to stimulate JHCO3- was not apparently dependent on mucosal Na+. Simultaneous addition of 10 mM Cl- to the Na+ -free mucosal medium and 10 mM Na+ to the Cl- -free serosal medium stimulated JHCO3- above levels produced by serosal Na+ alone. In conclusion, intestinal HCO3- secretion required mucosal Cl- and serosal Na+ and did not involve mucosal NaCl cotransport. The results are consistent with a mucosal Cl- absorptive mechanism in series with parallel basolateral Na+ -H+ and Cl- -HCO3- exchange mechanisms.
D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D002712:Chlorides / Q000494:pharmacology*; D004386:Duodenum / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D004553:Electric Conductivity; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D007700:Kinetics; D008564:Membrane Potentials; D012964:Sodium / Q000494:pharmacology; D014562:Caudata
D001639:Bicarbonates; D002712:Chlorides; D012964:Sodium