1. The effect of bisacodyl and oxyphenisation on the Na+-K+- and Mg2+-activated ATPase and on the mucosa levels of cAMP and cGMP was investigated in transporting ligated loops of the rat colon in acute studies and in chronic feeding experiments 2. The specific activity of the Na+-K+-ATPase was lowered in both types of experiments, concomitantly with a reduction in net sodium absorption. The specific activity of the Mg2+-activated ATPase was unaffected. 3. The cAMP content per mg protein was elevated and the cGMP content decreased in the acute experiments in which the effect on transport was most marked. The content of cyclic nucleotides returned to normal within 2 h whereas absorption, Na+-K+-ATPase specific activity and the mucosal potential difference were still significantly depressed at that time. In chronic experiments with bisacodyl, cAMP was not affected and cGMP was increased in colon loops exhibiting reduced absorption. 4. The results indicate that the inhibition of the Na+-K+-activated ATPase by diphenolic laxatives may play a role in the inhibition of intestinal fluid absorption caused by these compounds. The increase of cAMP in acute experiments could point to a cAMP-mediated stimulation of secretory processes under this condition.
SUMMARY1. Vasopressin enhanced the absorption of water and Na+ across everted sacs of rat colon descendens but had no effect on absorption across the colon ascendens. 3. Vasopressin increased the muscosal to serosal flux of Na+ and Cl-and decreased the serosal to mucosal flux ofCl-across short-circuited colon descendens. Consequently these changes increased the net flux of Na+ and Cl-.4. Adenylate cyclase activity in homogenates of the colon descendens was not altered by vasopressin.5. Omission of Ca2+ from the serosal bathing solution reversibly decreased 4, and p.d. and increased Na+ and Cl-absorption across the colon descendens in a similar way as did vasopressin. The results suggest that the effect of vasopressin on the colon descendens may be due to a decrease in intracellular Ca2+ activity.
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