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Delta-sleep-inducing peptide (DSIP) inhibited CRF-induced ACTH secretion from rat anterior pituitary gland in vitro

Study · animal · Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 1986 · DOI 10.1055/s-2007-1012357 · PMID 3017833

Plain-language summary

Paraphrased from the published abstract below — not a verdict on whether anything works.

In this rat study (in vitro, anterior pituitary quarters), delta-sleep-inducing peptide (DSIP) at 10(-9) - 10(-7) M significantly inhibited CRF-induced ACTH release from rat anterior pituitary tissue, with 10(-8) M DSIP showing the most prominent inhibition. DSIP at 10(-8) M also inhibited CRF-activated cAMP levels in anterior pituitary tissue but did not influence basal ACTH or cAMP levels. Prostaglandin E2 (PGE2) release from anterior pituitary quarters was not changed by DSIP. The authors conclude that DSIP inhibits CRF-induced ACTH release at the pituitary level through inhibition of the cAMP system in corticotrophs, and state that involvement of PGE2 in this phenomenon is unlikely.

Abstract

Delta-sleep-inducing peptide (DSIP, 10(-9) - 10(-7) M) significantly inhibited the CRF-induced ACTH release from rat anterior pituitary quarters in vitro. 10(-8) M DSIP showed the most prominent inhibition. DSIP (10(-8) M) also inhibited the CRF-activated cAMP levels in anterior pituitary tissue. DSIP did not influence basal ACTH or cAMP levels. Prostaglandin E2 (PGE2)-release from anterior pituitary quarters was not changed by DSIP. From these results, we conclude that DSIP inhibits CRF-induced ACTH release at the pituitary level through the inhibition of the cAMP system in corticotrophs. The involvement of PGE2 in this phenomenon is unlikely.

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