Role of prostaglandins and cAMP in the secretory effects of cholera toxin

The role of adenosine 3′,5′-monophosphate (cAMP) and prostaglandins in the pathogenesis of experimental cholera was evaluated. Fluid accumulated in the rabbit intestinal loop model after 16 hours of incubation with cholera toxin, prostaglandin E₁, or prostaglandin E₂, but not with membrane-permeable derivatives of cAMP or forskolin. Dibutryl cAMP triggered a small, transient intestinal fluid accumulation response by 4.5 hours; however, the fluid was completely absorbed by 9 hours. After exposure of intestinal loops to cholera toxin, prostaglandin E was released into the intestinal lumen in a concentration-dependent manner independent of cAMP. Thus, not only cAMP, but also prostaglandins may regulate water and electrolyte secretion in cholera.