β-Endorphin Attenuates the Serum Cortisol Response to Exogenous Adrenocorticotropin

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Abstract
Controversy surrounds the issue of whether β-endorphin affects adrenal steroidogenesis. Recent work has both supported and refuted the claim that β-endorphin stimulates a rise in serum aldosterone. We investigated the role of β-endorphin in adrenal steroidogenesis by examining its potential modulation of the response of serum cortisol to exogenous ACTH (Cosyntropin). Four or five normal men received: 1) synthetic β-endorphin (1 μg/kg·min) for 30 min, followed by a bolus dose of 0.2 μg ACTH; 2) β-endorphin (100 μg, iv), followed by 0.2 μg ACTH iv; 3) 0.2 μg ACTH iv; and 4) β-endorphin (100 μg iv) alone. The integrated cortisol response to exogenous ACTH, calculated as the area under the cortisol response curve, was significantly less when the ACTH infusion was preceded by the 30-min β-endorphin infusion than when administered alone [163 ± 50 (SE) μg/dl. min vs. 282 ± 51 μg/dl · min, respectively; P < 0.01]. By contrast, there was no difference between the integrated cortisol response to exogenous ACTH alone and exogenous ACTH after the bolus dose of β-endorphin (282 ± 51 vs. 293 ± 39 μg/dl · min, respectively).β-Endorphin (30-min infusion or 100-μg bolus dose alone) caused no change in serum aldoste-rone, dehydroepiandrosterone, or PRA. Serum PRL levels, however, were raised significantly (P < 0.05) by the 30-min infusion of β-endorphin. The infusion and bolus doses of β-endorphin raised plasma β-endorphin levels to over 100,000 pg/ml and 5,000 pg/ml, respectively. We conclude that very high plasma levels of β-endorphin may influence the response of cortisol to ACTH through a direct effect on the adrenal cortex. However, even in disease states such as Addison's and Nelson's diseases, such levels of plasma β-endorphin are not known to be achieved.