MECHANISMS OF OXALATE ABSORPTION AND SECRETION ACROSS THE RABBIT DISTAL COLON

To further evaluate the mechanisms of oxalate (Ox(2-)) transport in the intestine the following studies were performed using isolated, short-circuited segments of the rabbit distal colon (DC). In control buffer, the DC absorbed Ox(2-) (net Ox(2-) flux, J(Net)(Ox) = 5.4 +/- 0.7 pmol.cm(-2).h(-1)). Replacement of Na+ with N-methyl-D-glucamine (NMDG(+)) abolished Ox(2-) absorption by decreasing mucosal to serosal Ox(2-) flux (J(ms)(Ox)), without affecting Cl- transport, while gluconate substitution for Cl- did not affect J(Net)(Ox) or net Na+ flux (J(Net)(Na)). Addition of Na+ to the serosal side of tissues bathed by NMDG(+) buffer increased J(ms)(Ox) 40% without altering mucosal to serosal Cl- flux (J(ms)(Cl)). Serosal amiloride or dimethyl amiloride (10(-3) M) abolished J(Net)(Ox) by decreasing J(ms)(Ox), it increased serosal to muscosal Cl- flux (J(sm)(Cl)) and it gradually inhibited short-circuit current (I-sc). Mucosal amiloride (10(-4) M) abolished I-sc but had no effect on Ox(2-) or Cl- fluxes. Serosal 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS, 10(-6) M) reduced J(ms)(Ox) by 20% and J(Net)(Ox) by 43% without affecting J(ms)(Cl) or J(Net)(Cl). Dibutyryl cyclic adenosine monophosphate (dB-cAMP, 5 X 10(-4) M, both sides) stimulated Ox(2-) secretion (J(Net)(Ox) = -12.6 +/- 3.3 pmol.cm(-2) h(-1)). The dB-cAMP-induced secretion of Ox(2-) and Cl- were fully abolished by serosal furosemide (10(-4) M) and partially inhibited (35%) by 5 X 10(-4) M mucosal NPPB [5-nitro-2-(3-phenylpropylamino)-benzoic acid], a putative Cl- channel blocker. It is proposed that: (1) basal absorption of Ox(2-), but not Cl-, is dependent upon a previously undescribed basolateral Na+-H+ exchanger that may be coupled to a DLDS-sensitive, basolateral anion exchange system that mediates Ox(2-) flux; (2) the DC secretes Ox(2-) in response to dB-cAMP by a mechanism that is indistinguishable from the pathway for Cl- secretion.