Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-2-16
pubmed:abstractText
We sought to explain decreased ACTH secretory responses to stress in pregnant rats by investigating hypothalamic CRH and vasopressin secretion and actions on anterior pituitary corticotrophs. In late pregnancy median eminence, CRH content was reduced (by 12%). Anterior pituitary proopiomelanocortin mRNA expression, measured by in situ hybridization but not radioimmunoassayed ACTH content, was also reduced (by 45% on d 21); CRH receptor (CRHR)1 mRNA expression was unaltered in pregnancy, but V1b receptor mRNA expression was reduced (by 19%). ACTH secretory responses, measured in jugular blood, to CRH (200 ng/kg iv) or vasopressin (1.7 microg/kg, iv) were reduced on d 21 vs. virgins (49% and 44%), but the response to combined CRH and vasopressin injection was intact. Either antalarmin (CRHR1 antagonist; 20 mg/kg ip) or dP(Tyr(Me)2),Arg-NH2(9))AVP (V1a/b antagonist; 10 microg/kg, iv) pretreatment reduced the ACTH secretory response to forced swimming (90 sec) in virgin rats (by 57% and 40%), but only antalarmin was effective in pregnant rats (53% decrease). In vitro, measuring ACTH secretion from acutely dispersed anterior pituitary cells showed increased corticotroph sensitivity in pregnancy to CRH and to CRH augmentation by vasopressin, attributable to increased intracellular cAMP action. Hence, in late pregnancy, reduced anterior pituitary CRHR1 or V1b receptor expression did not impair corticotroph responses to CRH or vasopressin. Rather, diminished secretagogue secretion in vivo accounts for reduced action of stress levels of exogenous CRH or vasopressin alone; the late pregnancy attenuated ACTH secretory response to swim stress is deduced to be due to reduced vasopressin release by parvocellular paraventricular nuclei neurones.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
146
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1626-37
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15591137-Adrenocorticotropic Hormone, pubmed-meshheading:15591137-Animals, pubmed-meshheading:15591137-Dose-Response Relationship, Drug, pubmed-meshheading:15591137-Female, pubmed-meshheading:15591137-Hypothalamus, pubmed-meshheading:15591137-In Situ Hybridization, pubmed-meshheading:15591137-Pregnancy, pubmed-meshheading:15591137-Pregnancy, Animal, pubmed-meshheading:15591137-Pro-Opiomelanocortin, pubmed-meshheading:15591137-Pyrimidines, pubmed-meshheading:15591137-Pyrroles, pubmed-meshheading:15591137-RNA, Messenger, pubmed-meshheading:15591137-Radioimmunoassay, pubmed-meshheading:15591137-Rats, pubmed-meshheading:15591137-Rats, Sprague-Dawley, pubmed-meshheading:15591137-Receptors, Corticotropin-Releasing Hormone, pubmed-meshheading:15591137-Receptors, Vasopressin, pubmed-meshheading:15591137-Time Factors, pubmed-meshheading:15591137-Vasopressins
pubmed:year
2005
pubmed:articleTitle
Reduced hypothalamic vasopressin secretion underlies attenuated adrenocorticotropin stress responses in pregnant rats.
pubmed:affiliation
Centre for Integrative Physiology, School of Biomedical and Clinical Laboratory Sciences, College of Medicine and Veterinary Medicine, University of Edinburgh, Hugh Robson Building, George Square, Edinburgh, Scotland EH8 9XD, United Kingdom.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't