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Biomedical subjects

H Estep

Publications and source records attributed to H Estep.

6 recordsLinked to original sources
PubMed1988

Adrenocorticotropin and cortisol-induced changes in urinary sodium and potassium excretion in man: effects of spironolactone and RU486.

The role of the glucocorticoid (type II) receptor in the Na+ retention induced by cortisol is not known. The relative contribution of mineralocorticoid (type I) and type II receptor activation to changes in urinary Na+ and K+ excretion in man was studied using spironolactone and RU486 to inhibit type I and II receptors, respectively. Normal men eating a constant daily diet received either ACTH or cortisol for 5 days. Spironolactone (400 mg/day) inhibited ACTH (80 U/day)-induced kaliuresis, but not the Na+ retention produced by ACTH or cortisol (240 mg/day) and only blunted the modest Na+ retention induced by cortisol (120 mg/day). RU486 (1200 mg/day for the first 2 day) inhibited the first day kaliuresis and carbohydrate intolerance produced by cortisol, but did not affect the Na+ retention. Thus, the kaliuresis produced by cortisol and ACTH can be attributed to type II and type I receptor activation, respectively. The failure of RU486 to inhibit the Na+ retention induced by cortisol with evidence of adequate blockade of type II receptors indicates that the Na+ retention produced by cortisol is not mediated by type II receptor activation, but is, at least in part, mediated by the type I receptor.

Adrenocorticotropic Hormone↗
PubMed1986

Pseudo-Addison's disease. Isolated corticotropin deficiency associated with hyporeninemic hypoaldosteronism.

A 60-year-old man presented with loss of weight and appetite, eosinophilia, and hyperkalemia consistent with a diagnosis of Addison's disease. Adrenal responsiveness to exogenous corticotropin was normal, but endogenous corticotropin and cortisol responses to insulin-induced hypoglycemia were both absent. Pituitary function was otherwise intact. Renin and aldosterone levels were subnormal and did not respond to postural change. To our knowledge, this is the first reported case of isolated corticotropin deficiency and hyporeninemic hypoaldosteronism together mimicking primary adrenocortical failure.

Addison Disease↗
PubMed1977

Chloride-transport stimulatory factor in urine of chronically sodium-chloride loaded man.

Urinary extracts (in methylene dichloride) of subjects on high sodium-chloride (NaCl) intake produce net Cl- efflux (active transport) in isolated short-circuited frog skin. Activity is not found in the urine of NaCl-deprived normal subjects or NaCl-loaded subjects with adrenal insufficiency. These findings suggest that presence of an adrenocortical steriod which participates in adaptation to high salt intake. We describe here a lipid-soluble factor extracted from urine of chronically salt-loaded subjects which stimulates active Cl- transport in isolated frog skin. Our findings indicate that the factor is of adrenal origin and that it induces active ion transport in the direction opposite to that stimulated by the adrenal hormone, aldosterone. Aldosterone produces NaCl conservation in states of salt deprivation. We expect this new factor to produce NaCl excretion in states of excess salt ingestion.

Adrenal Cortex Hormones↗