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The primary recognized physiological action of aldosterone in man is the regulation of sodium homeostasis. This potent salt-retaining, adrenal hormone acts on the renal tubules to enhance sodium reabsorption (1-5). In addition, it has been established that aldosterone influences sodium transport in the salivary (1, 6-8) and sweat glands (7, 8). Whether aldosterone influences sodium absorp-tion from the human intestine has not been di-rectly measured but has been postulated on the basis of indirect evidence and animal studies (5, 9-19). Berger and Steele (11) demonstrated that the amount of sodium removed from the gut when a cation exchange resin was fed orally was considerably less in patients with congestive heart failure and decompensated cirrhosis (both condi-tions in which aldosterone secretion is increased) than in normal controls. Emerson, Kahn, and Jenkins (12) showed that during continued oral binding resin therapy in subjects on a low sodium intake a gradual decline in sodium output in the stools occurred. Laragh (5) reported that aldos-terone depresses the fecal Na/K ratio. Wong, Morrison, and Hurst (14) reported similar find-ings after oral administration of 9-fluorohydro-cortisone and in a patient with primary hyper-aldosteronism. * Submitted for publication September 29, 1964; ac-cepted January 21, 1965. This investigation was supported in part by U. S.
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Levitan et al. (1965) studied this question.
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