Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

The canine colonic epithelium can be stimulated by a variety of agonists. Increases in short-circuit current (Isc) can be rapidly reversed by serosal addition of PGD2 and one of its metabolites, 13,14 dihydro-15 keto PGD2 (DK). Although qualitatively similar effects were seen with a variety of agonists, those requiring calcium appeared to be affected more significantly. We have explored the posssibility that a calcium entry step on the serosal side could be the locus of the inhibitory effect. Tissues were set up in Ussing chambers and Iscs recorded. Removal of serosal Ca significantly reduced responses to carbachol and cyclopiazonic acid (CPA) but not forskolin. Replacement of calcium restored these responses. We assessed the ability of DK to reduced the restoration index (ratio of responses in calcium replaced solutions to serosal calcium-free solutions). For comparative purposes we used verapamil( an L-type Ca channel blocker) and Nickel (a mixed T-type, non-specific cation channel blocker). Nickel markedly inhibited responses to all 3 agonists. However verapamil and DK only affected carbachol induced responses. We constructed concentration-response curves to calcium added to CPA-treated tissues. Under these conditions, both DK and nickel exhibited marked inhibitory effects. Both produced significant reductions in maximal responses and nickel also produced a significant right-ward shift. The data suggest that a calcium entry step may be one potential locus for the prostaglandin effects but also indicate complexities in the sources of calcium in maintaining stimulation by agonists. (Supported by MRC Canada)

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Poster Number PAschleihauf0824
Keywords: epithelia, ion transport, calcium channel, prostaglandins