Aim: 

The study was aimed at affirming the direct negative feedback of cortisol on adrenal steroidogenesis at adrenocortical level in humans.

Methods: 

Ten young healthy women in the phollicular phase underwent four tests. In the repeated minimal ACTH-ACTH test, dose of 1mg of ACTH was administered intravenously twice: at 9am and 10am, respectively. The control test consisted of single ACTH administration at 10am. In the HC-ACTH test, 20mg of hydrocortisone (HC) was given per os and 1mg of ACTH was injected intravenously 90min after the HC administration. The control test with sole HC administration was performed.

Results: 

The first ACTH administration in the ACTH-ACTH test caused a significant increase of plasma cortisol concentration. The cortisol response after the subsequent ACTH bolus was present (Dmax: 180.8 ± 27.5 nmol/l, p < 0.001), but significantly lower (p < 0.011) than after the first ACTH administration (Dmax: 280.7 ± 12.8 nmol/l, p < 0.001). Responses of the other adrenal steroids 17a-OH-progesterone, D4-androstenedione and dehydroepiandrosterone after both ACTH administrations were comparable. ACTH administration during HC-induced hypercortisolemia maintained a plateau in cortisol concentration and prevented a decrease in cortisol level at this timepoint, which was seen after the HC administration alone. As known, the levels of the cortisol precursors decreased after the HC administration, followed by a significant rise after the ACTH bolus.

Conclusions: 

Pharmacologically induced hypercortisolemia does not suppress the cortisol secretion from adrenals and does not influence the adrenal steroidogenesis. The present study suggests that there is not a direct inhibitory effect of cortisol on steroidogenesis on adrenocortical level in humans. Supported by VEGA 2/6157/27.