Stimulation of Adrenocorticotropin/β-Endorphin Release by Synthetic Ovine Corticotropin-Releasing Factor in vitro

Publisher Website
Google Scholar
Abstract
Vasopressin analogs, which markedly differed in the ratio of pressor versus antidiuretic activity and also in ACTH/β-endorphin-releasing activity, were used in the present study. The ability of vasopressin and these analogs to enhance the release of adrenocorticotropin- (ACTH-IR) and β-endorphin-like immunoreactivity (β-EI) induced by synthetic ovine corticotropin-releasing factor –CRF–(1–41)– was studied in vitro using incubated rat anterior pituitary quarters. Arginine vasopressin (AVP) potentiated the action of CRF-(1–41) 2- to 4-fold. Vasopressin analogs, which possess direct CRF-like activity when given alone, also enhanced β-EI release caused by CRF-(1–41); the lowest concentration able to potentiate CRF-(1–41) activity was closely correlated with the EDso value of these analogs for direct CRF-like activity. The vasopressin analog 1-(β-mercapto-β, β-cyclopentamethylenepropionic acid)-2-(O-methyl)tyrosine-8-arginine-vasopressin blocked the release of ACTH-IR induced by AVP; however, this analog failed to prevent the potentiation by AVP of ACTH-IR release caused by CRF-(1–41), but enhanced itself the action of CRF-(1–41). Two analogs, which exhibited no direct CRF-like activity and which also did not antagonize the CRF-like activity of AVP, markedly enhanced the ACTH-IR and β-EI response to CRF-(1–41). These data indicate that the potency of vasopressin analogs to enhance the action of CRF-(1–41) is not related to their reported vasopressor or antidiuretic activity and provide some evidence that the structural requirements for potentiation by vasopressin of CRF-(1–41) action may be different also from those parts of the vasopressin molecule which confer the ability to induce ACTH-IR/β-EI release in the absence of CRF-(1–41).

This publication has 23 references indexed in Scilit: