Effects of bisacodyl on cAMP and prostaglandin E2 contents, (Na + K) ATPase, adenyl cyclase, and phosphodiesterase activities of rat intestine

The hypothesis that bisacodyl induces inotestinal fluid accumulation by increasing mucosal PGE2 content, inhibiting (Na + K) ATPase, and stimulating adenyl cyclase activities was tested in rats. Eighteen hours after its intragastric administration, bisacodyl (5.9 mg/kg body wt) decreased significantly jejunal and colonic (Na + K) ATPase activity: 36.4 +/- 1.4 (SE) and 28.3 +/- 1.4, respectively, as compared to 42.1 +/- 1.6 and 37.0 +/- 2.9 mumol/mg protein/hr in saline-treated rats. Bisacodyl administration increased significantly jejunal and colonic PGE2 content and stimulatd jejunal and colonic adenyl cyclase activity as compared to those in control rats. Jejunal and colonic cAMP content was not significantly increased by bisacodyl. Four hours after its administration, bisacodyl increased intestinal PGE2 content but failed to stimulate adenyl cyclase activity. Pretreatment with indomethacin prevented the increase in PGE2 content and the stimulation of adenyl cyclase induced by bisacodyl. Only jejunal phosphodiesterase activity was stimulated by bisacodyl (10 mg/kg body wt). The results reported thus suggest that intestinal inhibition of (Na + K) ATPase activity, increase of mucosal PGE2 content, and possibly also stimulation of adenyl cyclase activity might contribute to the net water accumulation induced by bisacodyl. It is also suggested that the stimulation of adenyl cyclase activity is mediated by increase in mucosal PGE2 content.