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Heinrich M. Schulte and Bruno Allolio


The existence of a short-loop feedback inhibition of pituitary ACTH release by administration of β-endorphin was postulated. However, data on the effect of peripherally administered β-endorphin in humans are highly controversial. We infused human synthetic β-endorphin at a constant rate of 1 μg · kg−1 · min−1 or normal saline to 7 normal volunteers for 90 min. Thirty min after starting the β-endorphin or placebo infusion, releasing hormones were injected as a bolus iv (oCRH and GHRH 1 μg/kg, GnRH 100 μg, TRH 200 μg) and blood was drawn for measurements of β-endorphin immunoreactivity, all other pituitary hormones, and cortisol. Infusion of β-endorphin resulted in high β-endorphin plasma levels with a rapid decrease after the infusion was stopped. During the control infusion, β-endorphin plasma levels rose in response to CRH. Plasma ACTH and serum cortisol levels in response to the releasing hormone were not different in subjects infused with β-endorphin or placebo. The PRL response to TRH was significantly higher after β-endorphin than after placebo (area under the stimulation curve 1209±183 vs 834±104 μg · 1−1 · h). There was no difference in the response of all other hormones measured. Our data on ACTH and cortisol secretion do not support the concept of a shortloop negative feedback of β-endorphin acting at the site of the pituitary.

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Bruno Allolio, Martin Oremus, Martin Reincke, Hans-Jörg Schaeffer, Werner Winkelmann, Georg Heck, and Heinrich M Schulte

Allolio B, Oremus M, Reincke M, Schaeffer H-J, Winkelmann W, Heck G, Schulte HM. High-dose progesterone infusion in healthy males: evidence against antiglucocorticoid activity of progesterone. Eur J Endocrinol 1995;133:696–700. ISSN 0804–4643

High concentrations of unbound cortisol in late pregnancy have been explained by the antiglucocorticoid activity of high progesterone levels. To further test this hypothesis we studied the effect of high-dose progesterone on baseline and corticotrophin-releasing hormone (CRH)-induced hormone secretion in humans. In a double-blind crossover study eight healthy male volunteers received either progesterone (0.714 mg · kg−1 · h−1 for 60 min followed by a dose of 0.45 mg · kg−1 · h−1 over a total infusion time of 315 min) or vehicle as a continuous intravenous infusion. At 210 min a CRH test (0.1 μg/kg body weight as bolus iv) was performed. Within 30 min after the start of progesterone administration the serum progesterone level increased to 454 ± 31 nmol/l and remained in the range of third trimester pregnancy concentrations throughout the infusion period. During vehicle infusion the progesterone level remained in the normal range for healthy males and demonstrated a small but significant increase after CRH (1.52 ± 0.23 vs 0.74 ± 0.14 nmol/l; p < 0.01). However, baseline and CRH-stimulated serum cortisol and plasma adrenocorticotrophic hormone remained unaffected by high-dose progesterone. Moreover, unbound salivary cortisol also was not affected by progesterone, suggesting that there is no significant competition for transcortin binding sites. In conclusion, no antiglucorticoid activity was found after short-term administration of progesterone in males. These findings cast doubts on the concept that the alterations of the pituitary–adrenal axis in late pregnancy are induced by the antiglucocorticoid activity of high progesterone concentrations.

Bruno Allolio, Medizinische Universitätsklinik Würzburg, Josef-Schneider-Str. 2, 97080 Würzburg, Germany