Three women in the fourth, seventh and eighth months respectively of normal pregnancy were given courses of intramuscularly administered progesterone in a dose of 50 or 100 mg. per day. In none of them was there a detectable influence on protein metabolism. In one, the 100-mg. course appeared to induce a mild natriuresis; no loss of sodium occurred in the others. These results contrast with the moderate catabolic response and distinct natriuresis observed regularly in normal subjects. Approximately 50 mg. daily of administered progesterone had previously been shown to elicit a maximal catabolic response. The failure of progesterone to be catabolic in pregnant women was explained by the assumption that endogenous progesterone was already inducing its maximal catabolic influences. The mild and inconstant natriuretic responses may have resulted from an inability of administered progesterone to inhibit sufficiently the influence of the increased amount of aldosterone present during pregnancy. IT HAS been shown that intramuscularly administered progesterone will increase the net rate of protein catabolism and enhance the urinary excretion of sodium and chloride in nonpregnant women and in men (1–3). This mild to moderate catabolic process can be distinguished qualitatively from those resulting from excesses of adrenocortical and thyroid hormones (2, 4). The natriuresis and chloruresis have been ascribed to an inhibition of the renal tubular effects of aldosterone and other sodium-retaining adrenal secretions (2, 5). The influence of progesterone on both protein and electrolyte metabolism was detectable when as little as 12.5 mg. per day was administered. The catabolic response was maximal at a daily dosage of about 25–50 mg., but the intensity and duration of the natriuresis continued to increase until a dosage level of at least 200–300 mg. per day had been reached (6).
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Landau et al. (1960) studied this question.
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