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 journal › Journal article › Research › peer-review
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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