Vasopressin pressor receptor-mediated activation of HPA axis by acute ethanol stress in rats

Author:

László Ferenc A.1,Varga Csaba1,Pávó Imre2,Gardi János2,Vecsernyés Miklós2,Gálfi Márta2,Morschl Éva3,László Ferenc3,Makara Gábor B.3

Affiliation:

1. Department of Comparative Physiology, Attila József University of Sciences, H-6726 Szeged;

2. Endocrine Unit and Research Laboratory, Albert Szent-Györgyi Medical School, H-6721 Szeged; and

3. Institute of Experimental Medicine, Hungarian Academy of Sciences, H-1083 Budapest, Hungary

Abstract

The plasma arginine vasopressin (AVP), ACTH, and corticosterone levels and the hypothalamic corticotropin-releasing hormone (CRH) content were measured after oral administration of 1 ml of 75% ethanol to rats, a model known to induce acute gastric erosions and stress.Elevated plasma AVP, ACTH, and corticosterone levels were detected 1 h after ethanol administration. Treatment with the vasopressin pressor (V1) receptor antagonist [d(CH2)5Tyr(Me)-AVP] before ethanol administration significantly reduced the ACTH and corticosterone level increases. A higher hypothalamic CRH content was measured at 30 or 60 min after ethanol administration. V1receptor antagonist injection, 5 min before ethanol administration, inhibited the rise in hypothalamic CRH content. The protein synthesis blocker cycloheximide prevented the hypothalamic CRH content elevation after stress. The AVP-, CRH-, and AVP + CRH-induced in vitro ACTH release in normal anterior pituitary tissue cultures was also prevented by pretreatment with the V1receptor antagonist.The results support the hypothesis that stress-induced AVP may not only act directly on the ACTH producing anterior pituitary cells but also indirectly at the hypothalamic level via the synthesis and release of CRH.

Publisher

American Physiological Society

Subject

Physiology (medical),Physiology

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