Involvement of vasopressin v1- and v2-receptors in histamine-and stress-induced secretion of ACTH and β-endorphin

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Involvement of vasopressin v1- and v2-receptors in histamine-and stress-induced secretion of ACTH and β-endorphin. / Kjær, Andreas; Knigge, Ulrich; Vilhardt, Hans; Bach, Flemming W.; Warberg, Jørgen.

In: Neuroendocrinology, Vol. 57, No. 3, 1993, p. 503-509.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Kjær, A, Knigge, U, Vilhardt, H, Bach, FW & Warberg, J 1993, 'Involvement of vasopressin v1- and v2-receptors in histamine-and stress-induced secretion of ACTH and β-endorphin', Neuroendocrinology, vol. 57, no. 3, pp. 503-509. https://doi.org/10.1159/000126398

APA

Kjær, A., Knigge, U., Vilhardt, H., Bach, F. W., & Warberg, J. (1993). Involvement of vasopressin v1- and v2-receptors in histamine-and stress-induced secretion of ACTH and β-endorphin. Neuroendocrinology, 57(3), 503-509. https://doi.org/10.1159/000126398

Vancouver

Kjær A, Knigge U, Vilhardt H, Bach FW, Warberg J. Involvement of vasopressin v1- and v2-receptors in histamine-and stress-induced secretion of ACTH and β-endorphin. Neuroendocrinology. 1993;57(3):503-509. https://doi.org/10.1159/000126398

Author

Kjær, Andreas ; Knigge, Ulrich ; Vilhardt, Hans ; Bach, Flemming W. ; Warberg, Jørgen. / Involvement of vasopressin v1- and v2-receptors in histamine-and stress-induced secretion of ACTH and β-endorphin. In: Neuroendocrinology. 1993 ; Vol. 57, No. 3. pp. 503-509.

Bibtex

@article{ed518f0abfd7463494c2d61b29f99a2c,
title = "Involvement of vasopressin v1- and v2-receptors in histamine-and stress-induced secretion of ACTH and β-endorphin",
abstract = "Arginine-vasopressin (AVP) seems to be involved in the histamine (HA)- and stress-induced release of ACTH and β-endorphin (β-END). We studied the effect of selective AVP V1- or V2-receptor blockade on the ACTH and β-END response to HA or restraint stress in conscious male rats. HA (270 nmol) administered intracerebroventricularly or 5 min of restraint stress caused a 3-to 7-fold increase in the plasma levels of ACTH and β-END immunoreactivity (β-ENDir). Pretreatment of the animals with the nonselective V1+2-receptor antagonist [l-Pmp-2-Z)-Phe-4-Ile-8-Arg]vasopressin, which was administered intravenously in a low (23 nmol) or a high dose (90 nmol) inhibited the HA-or restraint stress-induced secretion of ACTH and β-ENDir 60 and 25-70%, respectively. Pretreatment with equipotent doses of the selective V1-receptor antagonist [l-(p-tBu)Pmp-2-Tyr(0-Me)-8-D-Arg]vasopressin (25 nmol) and/or the selective V2-receptor antagonist [l-Pmp-2-D-IIe-4-Ile-8-Arg]vasopres-sin (7.0 nmol) attenuated the response of ACTH and β-ENDir to HA or restraint stress by 60-80 and 40-60%, respectively. In general, these doses of antagonists had no effect on basal hormone levels. We conclude that AVP takes part in the mediation of HA- and restraint stress-induced ACTH and β-END secretion. This effect seems to be mediated via both AVP V1 and V2-receptors or a less selective receptor with ligand specificity for both V1- and V2-receptor antagonists.",
keywords = "ACTH, Histamine, Pro-opiomelanocortin, Stress, Vasopressin, Vasopressin antagonists, Vasopressin receptors, β-Endorphin",
author = "Andreas Kj{\ae}r and Ulrich Knigge and Hans Vilhardt and Bach, {Flemming W.} and J{\o}rgen Warberg",
year = "1993",
doi = "10.1159/000126398",
language = "English",
volume = "57",
pages = "503--509",
journal = "Neuroendocrinology",
issn = "0028-3835",
publisher = "S Karger AG",
number = "3",

}

RIS

TY - JOUR

T1 - Involvement of vasopressin v1- and v2-receptors in histamine-and stress-induced secretion of ACTH and β-endorphin

AU - Kjær, Andreas

AU - Knigge, Ulrich

AU - Vilhardt, Hans

AU - Bach, Flemming W.

AU - Warberg, Jørgen

PY - 1993

Y1 - 1993

N2 - Arginine-vasopressin (AVP) seems to be involved in the histamine (HA)- and stress-induced release of ACTH and β-endorphin (β-END). We studied the effect of selective AVP V1- or V2-receptor blockade on the ACTH and β-END response to HA or restraint stress in conscious male rats. HA (270 nmol) administered intracerebroventricularly or 5 min of restraint stress caused a 3-to 7-fold increase in the plasma levels of ACTH and β-END immunoreactivity (β-ENDir). Pretreatment of the animals with the nonselective V1+2-receptor antagonist [l-Pmp-2-Z)-Phe-4-Ile-8-Arg]vasopressin, which was administered intravenously in a low (23 nmol) or a high dose (90 nmol) inhibited the HA-or restraint stress-induced secretion of ACTH and β-ENDir 60 and 25-70%, respectively. Pretreatment with equipotent doses of the selective V1-receptor antagonist [l-(p-tBu)Pmp-2-Tyr(0-Me)-8-D-Arg]vasopressin (25 nmol) and/or the selective V2-receptor antagonist [l-Pmp-2-D-IIe-4-Ile-8-Arg]vasopres-sin (7.0 nmol) attenuated the response of ACTH and β-ENDir to HA or restraint stress by 60-80 and 40-60%, respectively. In general, these doses of antagonists had no effect on basal hormone levels. We conclude that AVP takes part in the mediation of HA- and restraint stress-induced ACTH and β-END secretion. This effect seems to be mediated via both AVP V1 and V2-receptors or a less selective receptor with ligand specificity for both V1- and V2-receptor antagonists.

AB - Arginine-vasopressin (AVP) seems to be involved in the histamine (HA)- and stress-induced release of ACTH and β-endorphin (β-END). We studied the effect of selective AVP V1- or V2-receptor blockade on the ACTH and β-END response to HA or restraint stress in conscious male rats. HA (270 nmol) administered intracerebroventricularly or 5 min of restraint stress caused a 3-to 7-fold increase in the plasma levels of ACTH and β-END immunoreactivity (β-ENDir). Pretreatment of the animals with the nonselective V1+2-receptor antagonist [l-Pmp-2-Z)-Phe-4-Ile-8-Arg]vasopressin, which was administered intravenously in a low (23 nmol) or a high dose (90 nmol) inhibited the HA-or restraint stress-induced secretion of ACTH and β-ENDir 60 and 25-70%, respectively. Pretreatment with equipotent doses of the selective V1-receptor antagonist [l-(p-tBu)Pmp-2-Tyr(0-Me)-8-D-Arg]vasopressin (25 nmol) and/or the selective V2-receptor antagonist [l-Pmp-2-D-IIe-4-Ile-8-Arg]vasopres-sin (7.0 nmol) attenuated the response of ACTH and β-ENDir to HA or restraint stress by 60-80 and 40-60%, respectively. In general, these doses of antagonists had no effect on basal hormone levels. We conclude that AVP takes part in the mediation of HA- and restraint stress-induced ACTH and β-END secretion. This effect seems to be mediated via both AVP V1 and V2-receptors or a less selective receptor with ligand specificity for both V1- and V2-receptor antagonists.

KW - ACTH

KW - Histamine

KW - Pro-opiomelanocortin

KW - Stress

KW - Vasopressin

KW - Vasopressin antagonists

KW - Vasopressin receptors

KW - β-Endorphin

UR - http://www.scopus.com/inward/record.url?scp=0027336437&partnerID=8YFLogxK

U2 - 10.1159/000126398

DO - 10.1159/000126398

M3 - Journal article

C2 - 8391663

AN - SCOPUS:0027336437

VL - 57

SP - 503

EP - 509

JO - Neuroendocrinology

JF - Neuroendocrinology

SN - 0028-3835

IS - 3

ER -

ID: 283516844