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The mechanism of apparently discrepant actions of glucocorticoids (GC) on GH secretion, in vivo suppression and in vitro potentiation, was studied in rats. Dexamethasone (Dex), at the concentration of 50 nmol/l, potentiated basal and GHRH-stimulated GH release from monolayer culture of normal rat pituitary cells in 48 h. On the other hand, in vivo administration of Dex, 165 micrograms daily for 3 days, consistently suppressed serum GH levels in female rats.

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A previously unidentified mineralocorticoid, 16beta-hydroxydehydroepiandrosterone (16beta OH-DHEA) has recently been isolated from urine extracts of patients with low-renin hypertension and reported to possess one-fortieth the mineralocorticoid potency of aldosterone by bioassay. However, using a radioreceptor assay, we demonstrate the affinity of 16beta-OH-DHEA for renal 3H-aldosterone receptors to be only 0.011 per cent that of unlabeled aldosterone.

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