In the present study the effects of intravenously administered corticotropin-releasing hormone (CRH) on the release of proopiomelanocortin (POMC) derivatives such as adrenocorticotropic hormone (ACTH), β-lipotropin (β-LPH) and β-endorphin (β-END) as well as direct effects of CRH on pain sensitivity were examined. In 16 healthy volunteers we studied the effects of 100 µg intravenously administered CRH in absence or presence of 12 mg naloxone on heat or pressure pain sensitivity, using a double-blind, cross-over and placebo-controlled design. To evaluate analgesic effects of CRH via release of POMC derivatives, we determined plasma concentrations of β-END-immunoreactive material (IRM), authentic β-END (β-END(1–31)) and β-LPH IRM, in parallel with heat and pressure pain tolerance thresholds before and 15 and 30 min after treatment with CRH (or placebo), and 5 min after naloxone (or placebo) administration which was administered 40 min after CRH (or placebo) injection. CRH increased levels of β-END IRM, β-END(1–31) and β-LPH IRM. As compared to β-END IRM levels measured by a commercial RIA kit, the β-END(1–31) levels determined by a highly specific two-site RIA, proved to be remarkably small. Furthermore, CRH did not induce increases of heat pain tolerance thresholds, but of pressure pain tolerance thresholds, which, however, were not reversible by naloxone. Neither β-END nor β-LPH IRM nor β-END(1–31) levels correlated with heat or pressure pain tolerance thresholds. We conclude that CRH does not modulate heat, but pressure pain; POMC derivatives like β-END IRM, β-END(1–31) or β-LPH do not mediate this effect.

fects of tourniquet-induced ischemia on the release of proopiomelanocortin derivatives determined in peripheral blood plasma.

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