Involvement of vasopressin v1- and v2-receptors in histamine-and stress-induced secretion of ACTH and β-endorphin
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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.
I: Neuroendocrinology, Bind 57, Nr. 3, 1993, s. 503-509.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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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