Histamine- and stress-induced prolactin secretion: Importance of vasopressin V1- and V2-receptors

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Histamine- and stress-induced prolactin secretion : Importance of vasopressin V1- and V2-receptors. / Kjaer, A.; Knigge, U.; Warberg, J.

In: European Journal of Endocrinology, Vol. 131, No. 4, 1994, p. 391-397.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Kjaer, A, Knigge, U & Warberg, J 1994, 'Histamine- and stress-induced prolactin secretion: Importance of vasopressin V1- and V2-receptors', European Journal of Endocrinology, vol. 131, no. 4, pp. 391-397. https://doi.org/10.1530/eje.0.1310391

APA

Kjaer, A., Knigge, U., & Warberg, J. (1994). Histamine- and stress-induced prolactin secretion: Importance of vasopressin V1- and V2-receptors. European Journal of Endocrinology, 131(4), 391-397. https://doi.org/10.1530/eje.0.1310391

Vancouver

Kjaer A, Knigge U, Warberg J. Histamine- and stress-induced prolactin secretion: Importance of vasopressin V1- and V2-receptors. European Journal of Endocrinology. 1994;131(4):391-397. https://doi.org/10.1530/eje.0.1310391

Author

Kjaer, A. ; Knigge, U. ; Warberg, J. / Histamine- and stress-induced prolactin secretion : Importance of vasopressin V1- and V2-receptors. In: European Journal of Endocrinology. 1994 ; Vol. 131, No. 4. pp. 391-397.

Bibtex

@article{301fda7919444d6e83c553ff4e3d2e16,
title = "Histamine- and stress-induced prolactin secretion: Importance of vasopressin V1- and V2-receptors",
abstract = "We investigated the involvement of arginine vasopressin (AVP) V1- and V2-receptors in the prolactin (PRL) secretory response to histamine (HA) or restraint stress stimulation in conscious male rats by selective blockade of AVP receptors using different antagonists. Histamine (270 nmol) administered intracerebroventricularly or 5 min of restraint stress stimulated PRL secretion 10-14-fold. Pretreatment with the selective V1-receptor antagonists [1-(p-t-butyl-β-mercapto-β,β-cyclopentamethylene propionic acid)-2-(O-methyl)tyrosine-8-arginine] vasopressin or [1-(β,-mercapto-β,β-cyclopentamethylene propionic acid)-2-(O-methyl)tyrosine-8-arginine]vasopressin inhibited the PRL response to HA and restraint stress in a dose-dependent manner with maximal inhibition of 60%. The effect of the two antagonists was identical when equipotent antivasopressor doses were administered. The selective V2-receptor antagonist [1-(β-mercapto-β, β-cyclopentamethylene propionic acid)-2-D-isoleucine-4-isoleucine-8-arginine]vasopressin was unable to inhibit the PRL response significantly. Combined administration of the V1-receptor antagonist [1-p-t-butyl-β-mercapto-β,β-cyclopentamethylene propionic acid)-2-O-methyl)tyrosine-8-D-arginine]vasopressin and the V2-receptor antagonist inhibited the PRL response to HA to the same extent as that observed when the V1-antagonist was administered alone. None of the antagonists used had any effect on basal PRL secretion. We conclude that AVP seems to play a role in the mediation of HA- and restraint stressinduced secretion of PRL, and that the AVP receptor involved is primarily of the V1-type or similar to this.",
author = "A. Kjaer and U. Knigge and J. Warberg",
year = "1994",
doi = "10.1530/eje.0.1310391",
language = "English",
volume = "131",
pages = "391--397",
journal = "Acta Endocrinologica, Supplement",
issn = "0804-4635",
publisher = "BioScientifica Ltd.",
number = "4",

}

RIS

TY - JOUR

T1 - Histamine- and stress-induced prolactin secretion

T2 - Importance of vasopressin V1- and V2-receptors

AU - Kjaer, A.

AU - Knigge, U.

AU - Warberg, J.

PY - 1994

Y1 - 1994

N2 - We investigated the involvement of arginine vasopressin (AVP) V1- and V2-receptors in the prolactin (PRL) secretory response to histamine (HA) or restraint stress stimulation in conscious male rats by selective blockade of AVP receptors using different antagonists. Histamine (270 nmol) administered intracerebroventricularly or 5 min of restraint stress stimulated PRL secretion 10-14-fold. Pretreatment with the selective V1-receptor antagonists [1-(p-t-butyl-β-mercapto-β,β-cyclopentamethylene propionic acid)-2-(O-methyl)tyrosine-8-arginine] vasopressin or [1-(β,-mercapto-β,β-cyclopentamethylene propionic acid)-2-(O-methyl)tyrosine-8-arginine]vasopressin inhibited the PRL response to HA and restraint stress in a dose-dependent manner with maximal inhibition of 60%. The effect of the two antagonists was identical when equipotent antivasopressor doses were administered. The selective V2-receptor antagonist [1-(β-mercapto-β, β-cyclopentamethylene propionic acid)-2-D-isoleucine-4-isoleucine-8-arginine]vasopressin was unable to inhibit the PRL response significantly. Combined administration of the V1-receptor antagonist [1-p-t-butyl-β-mercapto-β,β-cyclopentamethylene propionic acid)-2-O-methyl)tyrosine-8-D-arginine]vasopressin and the V2-receptor antagonist inhibited the PRL response to HA to the same extent as that observed when the V1-antagonist was administered alone. None of the antagonists used had any effect on basal PRL secretion. We conclude that AVP seems to play a role in the mediation of HA- and restraint stressinduced secretion of PRL, and that the AVP receptor involved is primarily of the V1-type or similar to this.

AB - We investigated the involvement of arginine vasopressin (AVP) V1- and V2-receptors in the prolactin (PRL) secretory response to histamine (HA) or restraint stress stimulation in conscious male rats by selective blockade of AVP receptors using different antagonists. Histamine (270 nmol) administered intracerebroventricularly or 5 min of restraint stress stimulated PRL secretion 10-14-fold. Pretreatment with the selective V1-receptor antagonists [1-(p-t-butyl-β-mercapto-β,β-cyclopentamethylene propionic acid)-2-(O-methyl)tyrosine-8-arginine] vasopressin or [1-(β,-mercapto-β,β-cyclopentamethylene propionic acid)-2-(O-methyl)tyrosine-8-arginine]vasopressin inhibited the PRL response to HA and restraint stress in a dose-dependent manner with maximal inhibition of 60%. The effect of the two antagonists was identical when equipotent antivasopressor doses were administered. The selective V2-receptor antagonist [1-(β-mercapto-β, β-cyclopentamethylene propionic acid)-2-D-isoleucine-4-isoleucine-8-arginine]vasopressin was unable to inhibit the PRL response significantly. Combined administration of the V1-receptor antagonist [1-p-t-butyl-β-mercapto-β,β-cyclopentamethylene propionic acid)-2-O-methyl)tyrosine-8-D-arginine]vasopressin and the V2-receptor antagonist inhibited the PRL response to HA to the same extent as that observed when the V1-antagonist was administered alone. None of the antagonists used had any effect on basal PRL secretion. We conclude that AVP seems to play a role in the mediation of HA- and restraint stressinduced secretion of PRL, and that the AVP receptor involved is primarily of the V1-type or similar to this.

UR - http://www.scopus.com/inward/record.url?scp=0028124423&partnerID=8YFLogxK

U2 - 10.1530/eje.0.1310391

DO - 10.1530/eje.0.1310391

M3 - Journal article

C2 - 7921229

AN - SCOPUS:0028124423

VL - 131

SP - 391

EP - 397

JO - Acta Endocrinologica, Supplement

JF - Acta Endocrinologica, Supplement

SN - 0804-4635

IS - 4

ER -

ID: 283516426