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The role of HCO₃^- in propionate-induced anion secretion across rat caecal epithelium.

ABSTRACT: Propionate, a metabolite from the microbial fermentation of carbohydrates, evokes a release of epithelial acetylcholine in rat caecum resulting in an increase of short-circuit current (I_sc) in Ussing chamber experiments. The present experiments were performed in order to characterize the ionic mechanisms underlying this response which has been thought to be due to Cl^- secretion. As there are regional differences within the caecal epithelium, the experiments were conducted at oral and aboral rat corpus caeci. In both caecal segments, the propionate-induced I_sc (I_Prop) was inhibited by > 85%, when the experiments were performed either in nominally Cl^-- or nominally HCO₃^--free buffer. In the case of Cl^-, the dependency was restricted to the presence of Cl^- in the serosal bath. Bumetanide, a blocker of the Na⁺-K⁺-2Cl^--cotransporter, only numerically reduced I_Prop suggesting that a large part of this current must be carried by an ion other than Cl^-. In the aboral caecum, I_Prop was significantly inhibited by mucosally administered stilbene derivatives (SITS, DIDS, DNDS), which block anion exchangers. Serosal Na⁺-free buffer reduced I_Prop significantly in the oral (and numerically also in aboral) corpus caeci. RT-PCR experiments revealed the expression of several forms of Na⁺-dependent HCO₃^--cotransporters in caecum, which might underlie the observed Na⁺ dependency. These results suggest that propionate sensing in caecum is coupled to HCO₃^- secretion, which functionally would stabilize luminal pH when the microbial fermentation leads to an increase in the concentration of short-chain fatty acids in the caecal lumen.

SUBMITTER: Ballout J

PROVIDER: S-EPMC8164622 | biostudies-literature |

REPOSITORIES: biostudies-literature

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