Opioid κ Receptors and the Secretion of Prolactin (PRL) and Growth Hormone (GH) in the Rat

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Abstract
The effects of bremazocine and U-50,488, two selective opioid Kreceptor agonists, and the preferential µ receptor agonist morphine on the secretion of PRL and GH were compared in conscious male rats bearing permanent right atrial cannulae for serial blood sampling and drug delivery. All three opioids stimulated PRL secretion in a dose-related manner, but the Kagonists differed from morphine in several respects. They were considerably more potent than morphine in triggering a PRL response, but were unable to elevate PRL levels to more than 100 ng/ml, whereas morphine, at the highest dose (4.5 mg/kg), induced an almost twice larger response. Also their PRL-releasing effect was inhibited more strongly by the preferential Kreceptor antagonist Mr-2266 than by naloxone, whereas Mr-2266 and naloxone, which are equipotent as antagonists of the µ receptors, were equipotent in suppressing the PRL-stimulating effect of morphine, a µ agonist. In a complete contrast to morphine, which effectively stimulated GH secretion, the Kagonists had no effect on GH release at lower doses and suppressed it at higher doses. It is concluded that the PRL-releasing effect of the Kagonists is mediated by the Kreceptors which may participate with the µ receptors in regulation of PRL secretion by opioids. The GH-inhibiting effect of the Kagonists requires further clarification.

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