Cholera toxin (CT) and prostaglandin E (PGE) increased the synthesis of 3′,5′-cyclic adenosine monophosphate (cAMP) in rabbit intestinal mucosa, which appeared to be responsible for inducing the release of 5-hydroxytryptamine (5-HT) from enterochromaffin cells into the intestinal lumen. With isolated intestinal cells, CT induced the synthesis of PGE more efficiently from epithelial cells than from lamina propria cells; however, the basal amount of this eicosanoid produced by lamina propria cells was approximately six-fold more than that formed by the epithelial cells. The CT-induced stimulation of arachidonate metabolism appeared to be generalised in nature, as PGF and leukotrienes were synthesised in addition to PGE. Injection of dibutyryl cAMP into the intestinal lumen markedly reduced both basal levels of PGE, as well as CT-induced levels of PGE, released into the luminal fluid. Similarly, when biopsy samples of tissue from rabbit intestinal loops, challenged with dibutyryl cAMP, were washed and incubated , the amount of PGE synthesis remained below basal levels. In contrast, when biopsy samples of normal small intestinal tissue were exposed to dibutyryl cAMP, PGE synthesis increased. Thus, cAMP appeared to down-regulate the levels of intestinal eicosanoids , despite its innate capacity to evoke PGE synthesis from mucosal tissue . Thus, the data indicate that CT-induced mediators exhibit interactive effects that alter their cellular concentrations, that in turn could affect the biological responses.


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