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

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Abstract

The plasma arginine vasopressin (AVP), ACTH, and corticosterone levels and the hypothalamic corticotropin-releasing hormone (CRH) content were measured after oral administration of I 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 I 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. V1 receptor 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 V1 receptor 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.

Original languageEnglish
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume280
Issue number2 49-2
Publication statusPublished - Feb 2001

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Vasopressin Receptors
Corticotropin-Releasing Hormone
Arginine Vasopressin
Ethanol
Pituitary Hormone-Releasing Hormones
Adrenocorticotropic Hormone
Corticosterone
Corticotrophs
Cycloheximide
Vasopressins
Oral Administration
Stomach
Injections

Keywords

  • Adrenocorticotropic hormone
  • Corticosterone
  • Hypothalamic corticotropin-releasing hormone
  • V receptor antagonist

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

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title = "Vasopressin pressor receptor-mediated activation of HPA axis by acute ethanol stress in rats",
abstract = "The plasma arginine vasopressin (AVP), ACTH, and corticosterone levels and the hypothalamic corticotropin-releasing hormone (CRH) content were measured after oral administration of I 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 I 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. V1 receptor 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 V1 receptor 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.",
keywords = "Adrenocorticotropic hormone, Corticosterone, Hypothalamic corticotropin-releasing hormone, V receptor antagonist",
author = "F. L{\'a}szl{\'o} and C. Varga and Imre P{\'a}v{\'o} and J. Gardi and M. Vecserny{\'e}s and M. G{\'a}lfi and E. Morschl and F. L{\'a}szl{\'o} and G. Makara",
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T1 - Vasopressin pressor receptor-mediated activation of HPA axis by acute ethanol stress in rats

AU - László, F.

AU - Varga, C.

AU - Pávó, Imre

AU - Gardi, J.

AU - Vecsernyés, M.

AU - Gálfi, M.

AU - Morschl, E.

AU - László, F.

AU - Makara, G.

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N2 - The plasma arginine vasopressin (AVP), ACTH, and corticosterone levels and the hypothalamic corticotropin-releasing hormone (CRH) content were measured after oral administration of I 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 I 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. V1 receptor 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 V1 receptor 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.

AB - The plasma arginine vasopressin (AVP), ACTH, and corticosterone levels and the hypothalamic corticotropin-releasing hormone (CRH) content were measured after oral administration of I 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 I 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. V1 receptor 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 V1 receptor 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.

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