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Studies of the Nature of the Interaction between Vasopressin and Corticotropin-Releasing Factor on Adrenocorticotropin Release in the Rat^*

CATHERINE RIVIER, JEAN RIVIER, PIERRE MORMEDE and WYLIE VALE

The Salk Institute La Jolla, California, 92037
The Laboratoire de Psychobiobgie des Comportements Adaptatifs, U259INSERM-INRA 33077 Bordeaux Cedex, France

Address requests for reprints to: Dr. Catherine Rivier, Peptide Biology Laboratory, The Salk Institute, P.O. Box 85800, San Diego, California 92138.

Abstract

Arginine-vasopressin (AVP) acts on vasocon-striction and diuresis through two different types of receptors (V₁ and V₂, respectively). Since AVP also modifies ACTH release, we have attempted to determine which class of receptors mediates the capacity of AVP to increase ACTH secretion and o t potentiate the effect of corticotropin-releasing factor (CRF) on the pituitary using two AVP antagonists: [1-deaminopenicil-lamine-2-(O-methyl)tyrosine]arginine-vasopressin [dPTyr(Me)-AVP], which blocks Vi receptors, and [1-(β-mercapto-β,β-cyclo-pentamethylene propionic acid)2-D-leucine-4-valine]arginine vasopressin [d(CH₂)₆DLeuValAVP], which interferes with V₂ receptors. dPTyr(Me)AVP, but not d(CH₂)₆DLeuValAVP, in-hibited the ACTH-releasing as well as the CRF-potentiating effects of both AVP and its antidiuretic analog [1-deamino-8-D-argininejvasopressin (dDAVP). These results suggest that the actions of AVP and dDAVP on the corticotrophs is primarily mediated through V₁ (pressor-like) receptors. (Endocrinology 115: 882–886, 1984)

Footnotes

^* This work was supported by NIH Grants AM-26741 and HD-13527 and a grant from The Rockefeller Foundation. Research was conducted in part by the Clayton Foundation for Research-California Division.

Investigator, Clayton Foundation.

Received November 17, 1983.

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