INVESTIGATIONS into the mechanisms of adrenal insufficiency have focussed on salt and water metabolism since Bauman and Kurland (1) first demonstrated electrolyte changes in the serum of adrenalectomized cats. The urinary loss of salt and the therapeutic effects of a high-salt diet or of desoxycorticosterone acetate in adrenal insufficiency in man and animal (2–7) led to the concept that one function of the adrenal cortex is to protect against the renal depletion of body sodium. Additional studies in animals emphasized this point of view by indicating a reduction during adrenal insufficiency of plasma volume (8) and extracellular fluids (9-15). Analysis of tissues secured during adrenal insufficiency indicated changes in the intracellular constituents as well (12, 15–19). The concept has been revised to include as part of the syndrome the movement of water and potassium intracellularly which, in combination with renal loss of sodium and retention of potassium, leads to further reduction in the extracellular fluids (20).
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Mendelsohn et al. (1955) studied this question.
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