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Effect of Fludrocortisone and Spironolactone on Sodium and Potassium Losses in Secretory Diarrhea

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Abstract

The response of the colon to aldosterone isbelieved to be an important adaptive mechanism toexcessive sodium losses in diarrhea. However, the degreeto which mineralocorticoid activity actually influences fecal output of sodium in people with diarrheais unknown. To gain insight into this question, 10normal people were treated with placebo, fludrocortisone(an aldosterone agonist), and spironolactone (an aldosterone antagonist) during threeexperimental periods lasting nine days. On days 5-8,diarrhea was induced by ingestion of phenolphthalein.Diet was controlled. Fecal sodium was 40 meq/day onplacebo and 29 meq/day on fludrocortisone, consistentwith mineralocorticoid stimulation of intestinal sodiumabsorption. However, contrary to our expectations,spironolactone therapy was also associated with a fall in fecal sodium output, to 28 meq/day. Toexplain this paradoxical effect of spironolactone, wesuggest that sodium depletion caused by spironolactone'snatriuretic action on the kidney caused the release of an unknown stimulant of intestinalsodium absorption, whose action more than overcame thereduced colonic absorption resulting from inhibition ofaldosterone activity by spironolactone. This interpretation implies that the intestinaladaptation to sodium depletion in diarrhea involves bothaldosterone and an aldosterone independent factor,working in concert to reduce fecal sodiumoutput.

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Wenzl, H.H., Fine, K.D., Ana, C.A.S. et al. Effect of Fludrocortisone and Spironolactone on Sodium and Potassium Losses in Secretory Diarrhea. Dig Dis Sci 42, 119–128 (1997). https://doi.org/10.1023/A:1018897307835

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