MODEL OF BICARBONATE SECRETION BY RESTING FROG STOMACH FUNDUS MUCOSA .1. TRANSEPITHELIAL MEASUREMENTS

In the present in vitro experiments on gastric fundus mucosa of Rana e sculenta we try to define the mechanism of alkaline secretion that is observed in summer frogs in the resting stomach (blockage of HCl secre tion by ranitidine, 10(-5) mol/l). The transepithelial voltage and th e rate of alkalinization (ASR) of an unbuffered gastric lumen perfusat e was measured as a function of serosal (and mucosal) fluid compositio n. ASR was high (0.88+/-S.E. 0.09 mu Eq.cm(-2) h(-1), n=11) during ser osal bath perfusion with HCO3--Ringer solution, decreased slightly to 0.50+/-0.07 mu Eq.cm(-2).h(-1) (n=6) in HCO3--free HEPES-buffered Ring er solution of the same pH, and decreased to approximately 20% when ca rbonic anhydrase was inhibited by acetazolamide. While replacement of mucosal or serosal Cl- did not - within 1 h - significantly alter ASR, replacement of serosal Na+ in the presence or absence of HCO-3 strong ly reduced ASR, and a similar reduction was observed after serosal app lication of the anion transport inhibitor DIDS (4,4-diisothiocyanatost ilbene-2,2-disulphonate, 2.10 mu mol/l), the metabolic poison rotenone (10(-5) mol/l), the uncoupler dinitrophenol (10(-4) mol/l), and the N a+ pump inhibitor ouabain (10(-4) mol/l), while serosal amiloride (10( -4) mol/l) had no effect. These data can be accounted for by a model o f alkaline secretion that consists of basolateral HCO3-- uptake from t he serosal fluid into the cell via a DIDS-inhibitable Na+(HCO3-)(n)-co transporter and HCO3- secretion from the cell to the gastric lumen via an anionic conductance pathway. Microelectrode experiments on oxyntop eptic cells reported in the subsequent paper suggest that these cells may also be involved in the resting state alkaline secretion.