Vasopressin as a neuroendocrine regulator of anterior pituitary hormone secretion

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Vasopressin as a neuroendocrine regulator of anterior pituitary hormone secretion. / Kjaer, A.

In: Acta Endocrinologica, Vol. 129, No. 6, 1993, p. 489-496.

Research output: Contribution to journalReviewResearchpeer-review

Harvard

Kjaer, A 1993, 'Vasopressin as a neuroendocrine regulator of anterior pituitary hormone secretion', Acta Endocrinologica, vol. 129, no. 6, pp. 489-496.

APA

Kjaer, A. (1993). Vasopressin as a neuroendocrine regulator of anterior pituitary hormone secretion. Acta Endocrinologica, 129(6), 489-496.

Vancouver

Kjaer A. Vasopressin as a neuroendocrine regulator of anterior pituitary hormone secretion. Acta Endocrinologica. 1993;129(6):489-496.

Author

Kjaer, A. / Vasopressin as a neuroendocrine regulator of anterior pituitary hormone secretion. In: Acta Endocrinologica. 1993 ; Vol. 129, No. 6. pp. 489-496.

Bibtex

@article{c2c16cd94ae44e339c0c3fb3143dd8e1,
title = "Vasopressin as a neuroendocrine regulator of anterior pituitary hormone secretion",
abstract = "Secretion of the anterior pituitary hormones adrenocorticotropin (ACTH), β-endorphin and prolactin (PRL) is complex and involves a variety of factors. This review focuses on the involvement of arginine-vasopressin (AVP) in neuroendocrine regulation of these anterior pituitary hormones with special reference to receptor involvement, mode of action and origin of AVP. Arginine-vasopressin may act via at least two types of receptors: V1- and V2-receptors, where the pituitary V1-receptor is designated V(1b). The mode of action of AVP may be mediating, i.e. anterior pituitary hormone secretion is transmitted via release of AVP, or the mode of action may be permissive, i.e. the presence of AVP at a low and constant level is required for anterior pituitary hormones to be stimulated. Under in vivo conditions, the AVP-induced release of ACTH and β-endorphin is mainly mediated via activation of hypothalamic V1-receptors, which subsequently leads to the release of corticotropin-releasing hormone. Under in vitro conditions, the AVP-stimulated release of ACTH and β-endorphin is mediated via pituitary V(1b)-receptors. The mode of action of AVP in the ACTH and β-endorphin response to stress and to histamine, which is involved in stress-induced secretion of anterior pituitary hormones, is mediating (utilizing V1-receptors) as well as permissive (utilizing mainly V1- but also V2-receptors). The AVP-induced release of PRL under in vivo conditions is conveyed mainly via activation of V1-receptors but V2-receptors and probably additional receptor(s) may also play a role. In stress- and histamine induced PRL secretion the role of AVP is both mediating (utilizing V1-receptors) and permissive (utilizing both V1- and V2-receptors). Arginine-vasopressin may be a candidate for the PRL-releasing factor recently identified in the posterior pituitary gland. Arginine-vasopressin of both magno- and parvocellular origin may be involved in the regulation of anterior pituitary hormone secretion and may reach the corticotrophs and the lactotrophs via three main routes: the peripheral circulation, the long pituitary portal vessels or the short pituitary portal vessels.",
author = "A. Kjaer",
year = "1993",
language = "English",
volume = "129",
pages = "489--496",
journal = "European Journal of Endocrinology",
issn = "0804-4643",
publisher = "BioScientifica Ltd.",
number = "6",

}

RIS

TY - JOUR

T1 - Vasopressin as a neuroendocrine regulator of anterior pituitary hormone secretion

AU - Kjaer, A.

PY - 1993

Y1 - 1993

N2 - Secretion of the anterior pituitary hormones adrenocorticotropin (ACTH), β-endorphin and prolactin (PRL) is complex and involves a variety of factors. This review focuses on the involvement of arginine-vasopressin (AVP) in neuroendocrine regulation of these anterior pituitary hormones with special reference to receptor involvement, mode of action and origin of AVP. Arginine-vasopressin may act via at least two types of receptors: V1- and V2-receptors, where the pituitary V1-receptor is designated V(1b). The mode of action of AVP may be mediating, i.e. anterior pituitary hormone secretion is transmitted via release of AVP, or the mode of action may be permissive, i.e. the presence of AVP at a low and constant level is required for anterior pituitary hormones to be stimulated. Under in vivo conditions, the AVP-induced release of ACTH and β-endorphin is mainly mediated via activation of hypothalamic V1-receptors, which subsequently leads to the release of corticotropin-releasing hormone. Under in vitro conditions, the AVP-stimulated release of ACTH and β-endorphin is mediated via pituitary V(1b)-receptors. The mode of action of AVP in the ACTH and β-endorphin response to stress and to histamine, which is involved in stress-induced secretion of anterior pituitary hormones, is mediating (utilizing V1-receptors) as well as permissive (utilizing mainly V1- but also V2-receptors). The AVP-induced release of PRL under in vivo conditions is conveyed mainly via activation of V1-receptors but V2-receptors and probably additional receptor(s) may also play a role. In stress- and histamine induced PRL secretion the role of AVP is both mediating (utilizing V1-receptors) and permissive (utilizing both V1- and V2-receptors). Arginine-vasopressin may be a candidate for the PRL-releasing factor recently identified in the posterior pituitary gland. Arginine-vasopressin of both magno- and parvocellular origin may be involved in the regulation of anterior pituitary hormone secretion and may reach the corticotrophs and the lactotrophs via three main routes: the peripheral circulation, the long pituitary portal vessels or the short pituitary portal vessels.

AB - Secretion of the anterior pituitary hormones adrenocorticotropin (ACTH), β-endorphin and prolactin (PRL) is complex and involves a variety of factors. This review focuses on the involvement of arginine-vasopressin (AVP) in neuroendocrine regulation of these anterior pituitary hormones with special reference to receptor involvement, mode of action and origin of AVP. Arginine-vasopressin may act via at least two types of receptors: V1- and V2-receptors, where the pituitary V1-receptor is designated V(1b). The mode of action of AVP may be mediating, i.e. anterior pituitary hormone secretion is transmitted via release of AVP, or the mode of action may be permissive, i.e. the presence of AVP at a low and constant level is required for anterior pituitary hormones to be stimulated. Under in vivo conditions, the AVP-induced release of ACTH and β-endorphin is mainly mediated via activation of hypothalamic V1-receptors, which subsequently leads to the release of corticotropin-releasing hormone. Under in vitro conditions, the AVP-stimulated release of ACTH and β-endorphin is mediated via pituitary V(1b)-receptors. The mode of action of AVP in the ACTH and β-endorphin response to stress and to histamine, which is involved in stress-induced secretion of anterior pituitary hormones, is mediating (utilizing V1-receptors) as well as permissive (utilizing mainly V1- but also V2-receptors). The AVP-induced release of PRL under in vivo conditions is conveyed mainly via activation of V1-receptors but V2-receptors and probably additional receptor(s) may also play a role. In stress- and histamine induced PRL secretion the role of AVP is both mediating (utilizing V1-receptors) and permissive (utilizing both V1- and V2-receptors). Arginine-vasopressin may be a candidate for the PRL-releasing factor recently identified in the posterior pituitary gland. Arginine-vasopressin of both magno- and parvocellular origin may be involved in the regulation of anterior pituitary hormone secretion and may reach the corticotrophs and the lactotrophs via three main routes: the peripheral circulation, the long pituitary portal vessels or the short pituitary portal vessels.

UR - http://www.scopus.com/inward/record.url?scp=0027787757&partnerID=8YFLogxK

M3 - Review

C2 - 8109180

AN - SCOPUS:0027787757

VL - 129

SP - 489

EP - 496

JO - European Journal of Endocrinology

JF - European Journal of Endocrinology

SN - 0804-4643

IS - 6

ER -

ID: 283516637