No abstract

The effect of dried senna pod extract, containing 10% sennoside B, on colonic electrolyte and fluid transport was examined in the anaesthetized rat in-situ. Oral administration of senna pod extract dose-dependently (17.5-30 mg kg-1, calculated as sennoside B) reversed net absorption of water, sodium and chloride to net secretion and increased potassium secretion. Senna pod extract stimulated the output of prostaglandin E2 into the colonic lumen. Inhibition of prostaglandin biosynthesis by pretreatment of the rats with indomethacin (10 mg kg-1) significantly inhibited the effects of senna pod extract (17.5-30 mg kg-1) both on net fluid transport and on prostaglandin E2 synthesis. The inhibitory effect of indomethacin on net fluid transport induced by senna pod extract (30 mg kg-1) was dose-dependent. It is concluded that anthraquinones exert their laxative action at least partially via stimulation of colonic fluid and electrolyte secretion, and that this secretion is mediated by stimulation of endogenous prostaglandin E2 formation.

The aim of this study was to investigate whether prostaglandins (PG) are involved in the mediation of sennoside-induced colonic fluid and electrolyte secretion. Oral administration of senna pod extract dose-dependently reversed net absorption of water, sodium and chloride to net secretion, increased potassium secretion and stimulated the release of PGE₂ into the colonic lumen. Inhibition of PG biosynthesis by pretreatment of the rats with indometacin significantly inhibited the effects of senna pod extract both on net fluid transport and on PGE₂ release. The inhibitory effect of indometacin on net fluid transport induced by senna pod extract was dose-dependent. It is concluded that sennosides exert their laxative action at least partially via stimulation of colonic fluid and electrolyte secretion, and that this secretion is mediated by stimulation of endogenous PGE₂ formation.