Abstract
Hydrogen sulfide (H2S) has recently been recognized as a gaseous signaling molecule that affects smooth muscle function. The aim of this study was to determine the effect of inflammation on the responses to H2S in smooth muscle of mouse colon. Colonic inflammation was induced by intracolonic administration of trinitrobenzene sulfonic acid (TNBS) in BALB/C mice. Isometric force was measured in the organ bath. In carbachol‐precontracted tissues, levcromakalim (LEV), a KATP channel opener, induced dose‐dependent relaxations (IC50 1036 nM, n=5). The dose‐response was shifted to the left in inflamed colon (IC50 458 nM, n=6). Similarly, relaxations to NaHS were also shifted to the left in the colitis model (control IC50 196 μM, n=6: inflamed IC50 151 μM, n=3) and maximal amplitude of relaxation was enhanced by 40%. Pretreatment with glybenclamide (100 uM) abolished LEV relaxations and reduced NaHS relaxations by 46 ± 8.2% (n=3). A Biotin switch assay was performed to determine s‐sulfyhdyration of SUR2B subunit of KATP. NaHS significantly enhanced sulfhyrdration of SUR2B in CHO transfected cells and in native colonic tissues. These data suggest that enhanced hydrogen sulfide during colitis, regulates contractile activity in the smooth muscle of mouse colon through S‐sulfhydration of the KATP channel. Supported by NIH DK046367.
Published Version
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