Importance of sodium intake and mineralocorticoid hormone in the impaired water excretion in adrenal insufficiency

In contrast to previous conclusions, the present results indicate that in the absence of adrenal hormones normal renal diluting ability may occur, indicating both maximal suppression of vasopressin release and maximal distal tubular impermeability to water

R. C. Ufferman; R. W. Schrier


Scholarcy highlights

  • There is considerable evidence that adrenal insufficiency is associated with an impaired ability to attain a normal water diuresis
  • One is that, the release of antidiuretic hormone' from the hypothalamus in adrenal insufficiency is normally suppressed during water loading, the water impermeability of the distal nephron is incomplete in the absence of glucocorticoid hormone
  • Utilization of the bioassay of ADH in adrenal insufficiency has not distinguished between these possible mechanisms, since evidence has been presented that ADH levels are both increased and undetectable in adrenal insufficiency
  • 'Abbreviations used in this paper: ADH, antidiuretic hormone; CHE2O, free-water clearance; Cosm, osmolar clearance; DOCA, deoxycorticosterone acetate; GFR, glomerular filtration rate; Uosm, urinary osmolality
  • In the presence of a liberal sodium intake the Uosm achieved during the acute water load in this animal was not altered by adrenalectomy, independent of adrenal steroid replacement
  • A further control observation was obtained during replacement of both glucocorticoid and mineralocorticoid hormone in the adrenalectomized state. Another aspect of the experimental design involved the use of physiological amounts of glucocorticoid hormone replacement rather than the larger doses of glucocorticoid hormone replacement which have been used previously to reverse the defect in water excretion in adrenal insufficiency .' In an effort to avoid any secondary effects related to negative sodium balance and depletion of extracellular fluid volume, the initial group of studies were performed while the animals were offered a high sodium intake as saline drinking water
  • The results of the present investigation must be considered on the background of the previous suggestions that the impaired renal diluting capacity characteristic of adrenal insufficiency is due to glucocorticoid deficiency and is mediated either by sustained release of antidiuretic hormone or by a failure to achieve maximal impermeability to water of the distal nephron

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