Abstract
WHEN progesterone is administered to men and women in a dosage approximating the quantity secreted during early pregnancy (50–100 mg. daily), it induces a mild to moderate acceleration of protein catabolism (1–4) and an increased excretion of urinary sodium and chloride (1, 2). The enhanced catabolism appears to be a metabolic effect of progesterone itself, but the salt-dissipating influence can be explained on the basis of an inhibition of salt-retaining adrenal corticoids at a renal level. In subjects with normal adrenals, the catabolic process seems less intense and the increase in the excretion of urinary sodium is distinctly smaller than the same effects induced in hormone-treated Addisonians. Furthermore, only in individuals with intact adrenal glands is the sodium loss promptly recovered after progesterone treatment is discontinued. Since the natriuresis and chloruresis induced by progesterone seem to be dependent upon a competitive reaction, the presence of adrenal hormones is required for this re...
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More From: The Journal of clinical endocrinology and metabolism
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