1989Journal of NeuroendocrinologyRequires access

Corticotrophin‐Releasing Factor Antagonist [alpha helical CRF(9–41)] Blocks Central Noradrenaline‐lnduced ACTH Secretion

Toshihiro Takao, Kozo Hashimoto, Ryuto Hirasawa, Shinya Makino, MASANORI SUGAWARA, Kazuharu Murakami, Zensuke Ota

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Abstract

Plasma ACTH increased after an intra-third ventricular administration of noradrenaline (NA). An iv corticotrophin-releasing factor (CRF) antagonist [alpha-helical CRF(9-41)] injection did not affect ACTH secretion by itself, whereas it significantly reduced NA-induced ACTH secretion. These results suggest that NA centrally stimulated ACTH secretion and that endogenous CRF is involved in this ACTH secretion.

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What this paper is about

Plasma ACTH increased after an intra-third ventricular administration of noradrenaline (NA). An iv corticotrophin-releasing factor (CRF) antagonist [alpha-helical CRF(9-41)] injection did not affect ACTH secretion by itself, whereas it significantly reduced NA-induced ACTH secretion. These results suggest that NA centrally stimulated ACTH secretion and that endogenous CRF is involved in this ACTH secretion.

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Available abstract

Plasma ACTH increased after an intra-third ventricular administration of noradrenaline (NA). An iv corticotrophin-releasing factor (CRF) antagonist [alpha-helical CRF(9-41)] injection did not affect ACTH secretion by itself, whereas it significantly reduced NA-induced ACTH secretion. These results suggest that NA centrally stimulated ACTH secretion and that endogenous CRF is involved in this ACTH secretion.

Key concepts: Endocrinology, Internal medicine, Secretion, Antagonist, ACTH secretion, Endogeny, Alpha (finance), Chemistry

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