Corticotropin-releasing hormone reduces pressure pain sensitivity in humans without involvement of beta-endorphin(1-31), but does not reduce heat pain sensitivity

Neuroendocrinology
Reginald MatejecHansjörg Teschemacher

Abstract

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), beta-lipotropin (beta-LPH) and beta-endorphin (beta-END) as well as direct effects of CRH on pain sensitivity were examined. In 16 healthy volunteers we studied the effects of 100 microg 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 beta-END-immunoreactive material (IRM), authentic beta-END (beta-END(1-31)) and beta-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 beta-END IRM, beta-END(1-31) and beta-LPH IRM. As compared to beta-END IRM levels measured by a commercial RIA kit, the beta-END(1-31) levels determined by a highly specific two-site RIA, proved to be remarkably sma...Continue Reading

Citations

Jan 12, 2012·Bulletin of Experimental Biology and Medicine·N I YarushkinaL P Filaretova
Oct 29, 2010·Journal of Cardiovascular Pharmacology·Reginald MatejecHeinz-Wilhelm Harbach
Sep 16, 2006·Peptides·Richard J Bodnar, Gad E Klein
Sep 24, 2019·Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences·Randolph M Nesse, Jay Schulkin

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