The role of volume‐sensitive CI channels in the stimulation of chloride absorption by short‐chain fatty acids in the rat colon

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Abstract
The short‐chain fatty acids acetate, propionate and butyrate induced a concentration‐dependent decrease in short‐circuit current (Isc) of the rat colonin vitro.The decrease inIsc, being more pronounced in the distal than in the proximal colon, was dependent on the presence of CI‐ions and partly on the presence of HCO‐3. In the distal colon, the fall inIsccould be inhibited by amiloride, indicating that the activity of the Na+/H+exchanger is necessary for the induction of this response. The decrease inIscwas diminished by the CI‐channel blocker, 5‐nitro‐2‐(3‐phenylpropylamino)‐benzoate, and the lipoxygenase inhibitor, nordihydroguaiaretic acid. In contrast, inhibitors of the leukotriene pathway or a CI‐channel blocker did not affect theIscresponse in the proximal colon.Measurements of unidirectional fluxes revealed that butyrate caused a stimulation of the mucosa to serosa fluxes (Jms) of Na+and CI‐in the distal, but only of jmsNain the proximal colon. Unidirectional Rb+fluxes were not altered. The stimulation of jmsclcorrelated with the degree of metabolism of the short‐chain fatty acid. The increase in jmsclwas most pronounced for butyrate, smaller for acetate and not observed with the poorly metabolizable short‐chain fatty acid, isobutyrate. Consequently, two factors seem to be responsible for the stimulation of CI‐absorption by short‐chain fatty acids in the distal colon: (1) the intracellular production of HCO‐3during the oxidation of short‐chain fatty acids as substrate for the apical Cr/HCO‐3exchanger, and (2) the activation of volume‐sensitive basolateral CI‐channels.

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