The TRH-metabolite histidyl-proline-diketopiperazine (DKP) inhibits prolactin secretion in male rhesus monkeys

Abstract

Abstract. Histidyl-proline-diketopiperazine (DKP) - a stable degradation product of TRH - has been shown to selectively inhibit prolactin secretion in vitro in rat pituitary tissue. In this study the effects of DKP on serum prolactin in intact and anaesthetized male rhesus monkeys and on TRH-stimulated prolactin levels have been investigated. In conscious monkeys 400 μg DKP significantly suppressed prolactin levels by 27%, and under ketamine anaesthesia, serum prolactin was suppressed in a dose-dependent manner by 150 and 400 μg DKP. The maximum prolactin response and the cumulative response to TRH (20 μg) was significantly and specifically inhibited by 400 μg DKP, while the lower dose was without effect. TSH levels were not affected by DKP in any instance. Hence DKP can specifically inhibit prolactin release in the rhesus monkey, and may be discussed as a possible regulatory factor in prolactin secretion.