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^Oxor net Na⁺ flux (J_Net^Na). Addition of Na⁺ to the serosal side of tissues bathed by NMDG⁺ buffer increased J_ms^Ox40% without altering mucosal to serosal Cl^– flux (J_ms^Cl). Serosal amiloride or dimethyl amiloride (10^–3 M) abolished J_Net^Oxby 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^Oxby 20% and J_Net^Oxby 43% without affecting J_ms^Clor J_Net^Cl. Dibutyryl cyclic adenosine monophosphate (dB-cAMP, 5×10^–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 5×10^–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 DIDS-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.