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Changes in the function and ionic composition of the alimentary tract in response to dietary cation deficiences, and the possible role of adrenal medullary and cortical hormones in mediating these responses Bass, Paul

Abstract

The possibility that loss of intestinal motility occurs as a result of potassium or sodium depletion has been investigated. A new technique, based on the passage of a solution containing the dye, gentian violet, was developed for estimating upper bowel motility. Lower bowel motility was not objectively studied. The sodium and potassium content of various portions of the gut from rats on a low sodium, low potassium diet and on a high sodium, low potassium diet have been determined and compared with that of similar portions of the gut of animals on a control diet. The possibility that excess adrenal cortical or medullary hormones may cause or permit electrolyte and motility changes has been studied. The response to dietary potassium restriction in the presence of a high sodium intake were also determined after adrenalectomy, both with and without medullory or cortical hormonal supplementation. The electrolyte pattern of plasma liver and of skeletal muscle from different portions of the body were analysed and compared in order to aid in understanding the overall electrolyte shifts. Analyses of the selected tissues of the body indicated that initial electrolyte concentrations and responses to diets and hormones vary within similar tissues as well as between different organs. It was not possible to correlate alterations in the gastro-intestinal tract content of sodium and/or potassium with changes in motility. Dietary potassium deprivation led to depletion of potassium only in plasma, skeletal muscle and certain portions of the gastro-intestinal tract in intact animals. This effect was prevented by adrenalectomy. Evidence is presented that cortisone can influence the electrolytes of the body by acting in the cells of peripheral tissues as well as on the kidney and that the high dose administered (4 mgm/day) had direct dietary potassium deficiency actions in addition to permitting depletion to occur in the presence of certain tissues. The hypothesis that excess adrenal cortical hormones cause intestinal immotility through loss of potassium or a gain of sodium in this tissue was not confirmed by the data. Evidence is presented indicating that adrenalin can partially restore the ability to excrete potassium and the ability of tissues to undergo potassium depletion in adrenalectomized animals on a potassium deficient diet. It does not correct the electrolyte levels in adrenalectomized animals on a control diets The possibility that adrenalin may play some role in maintaining electrolyte homeostatis is discussed.

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