Kinin-induced prostaglandin release in rat colon does not display serosal/mucosal ''sidedness'' after epithelial removal.

Release of prostaglandin E2 (PGE2) from rat colon in response to 1 microM lysylbradykinin (LBk) displayed 'sidedness' in preparations with an intact epithelial cell layer (PGE2 release, sensitivity to LBk and inhibition by indomethacin all occurred on the serosal side only). Preparations with histologically-verified removal of the epithelial layer and which were impermeable to prostaglandins (i.e. intact) continued to demonstrate LBk-induced PGE2 generation, but this and indomethacin inhibition did not display sidedness. The results show that kinin-induced PGE2 derives principally from cells in the lamina propria and not from the epithelial cells as previously supposed, and that the apparent sidedness of LBk responsiveness, PGE2 generation and its inhibition by indomethacin results from the barrier property of the epithelial cells and is not indicative of an asymmetric response.