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

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. (Endocrinology115: 882–886, 1984)