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A review of the recent progress in the study of the mode of action of the sennosides, the active constituents of the senna drug, is presented. An interaction between rhein anthrone, the active metabolite of the sennosides, and the immune cells of the colon is suggested as a base for laxative activity.

A review of the recent progress in the study of the mode of action of the sennosides, the active constituents of the senna drug, is presented. An interaction between rhein anthrone, the active metabolite of the sennosides, and the immune cells of the colon is suggested as a base for laxative activity.

Rhein (1,8-dihydroxy-3-carboxyanthraquinone), in a concentration of 6 X 10(-4)M, inhibits water absorption from the colon and causes a net transfer of fluid and electrolyte into the intestinal lumen. Morphine (4 X 10(-4)M) counteracted the water and electrolyte secretion. Prior perfusion with morphine protected the large intestine from the laxative effect of a rhein perfusion. Differences in absorption rate of 99mTc-EDTA, a poorly absorbable marker, were found, as morphine caused nearly all radioactive compound to be retained in the colon, while rhein significantly facilitated the transfer of marker from colon through mucosal barrier to blood. The route followed by the 99mTc-EDTA complex was not the same as that followed by water, suggesting that 99mTc-EDTA travels by a paracellular route. Morphine counteracted the inhibition of Na+ absorption caused by rhein and antagonized the massive loss of K+ incurred by the presence of rhein in the colon. Cl- absorption is reversed to secretion in the presence of rhein while normal values were restored by morphine. Neither the HCO-3 content nor the pH were affected by either drug. Active absorption of glucose was completely blocked in the presence of rhein; the block could be antagonized by morphine.