CHARACTERISTICS OF LUMINAL BICARBONATE SECRETION BY RAT CECUM INVITRO

Under in vitro conditions the rat cecum transported HCO3- from the serosal to an unbuffered solution in contact with the mucosal side [J(s-->m) = 7.12 +/- 0.18-mu-mol.cm-2.h-1 (n = 149)]. With reversed tissues, a significantly lower flux was obtained [J(m-->s) = 2.47 +/- 0.11 mu-mol.cm-2.h-1 (n = 42)]. Both fluxes were stable for several hours. Increasing the H+ gradient across the tissue for 60 min did not change either flux. Anoxia for 45 min reversibly reduced J(s-->m) by 65 +/- 3% (n = 20) but had no effect on J(m-->s). Both fluxes were linearly related to HCO3- concentration on the buffered side, but the slope for J(s-->m) was 3.5 times that for J(m-->s). When tissues were initially set up in HEPES buffer rather than HCO3-, J(s-->m) was 0.12 +/- 0.05-mu-mol.cm-2.h-1 (n = 6), which is not significantly different from zero. Replacement of Na+ by choline reduced J(s-->m) by 40 +/- 3% (n = 11) and ouabain (1 mM) by 24 +/- 3% (n = 5). Replacement of Cl- with isethionate or K+ with Na+ for 60 min did not alter J(s-->m). Serosal application of DIDS (0.5 mM) reduced J(s-->m) by 24 +/- 6% (n = 6), but SITS (0.5 mM), furosemide (1 mM), acetazolamide (0.1 mM), amiloride (1 mM), and a proton pump inhibitor (Sch 28080, 50-mu-M) had no effect. Mucosal application of DIDS, furosemide, and amiloride had no effect on J(s-->m). Serosal tetrodotoxin (1-mu-M) and indomethacin (28-mu-M) were also without effect. These results suggest that about one-third of J(s-->m) is due to passive diffusion of HCO3- and the remainder to an active transcellular transport process that is partly dependent on Na+.