Linked Life Data

10686522

Source:http://linkedlifedata.com/resource/pubmed/id/10686522

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2000-8-4
pubmed:abstractText
We have previously observed significant, albeit decreased, corticosterone responses to restraint stress in corticotropin releasing hormone (CRH)-deficient (knockout, CRH KO) mice. Because different stressors have been shown to engage different populations of hypophysiotropic neurons, we have used hypoglycemia and hypovolemia to test whether CRH-independent pituitary-adrenal activation is evoked by stimuli other than restraint. Insulin injection in fasted CRH KO mice elicited increases in corticosterone that were markedly lower than those in wild type but marginally significant relative to corresponding KO controls. Consistent with impaired adrenocortical function, hypoglycemia-induced epinephrine secretion was reduced in female CRH KO mice. Hypovolemia produced by retro-orbital bleeding also significantly elevated corticosterone in CRH KO mice. In contrast to significant stress-induced increases in corticotropin (ACTH) in wild-type mice, those in CRH KO mice were slight, transient and difficult to detect without frequent sampling. Restraint-induced interleukin-6 (IL-6) levels were similar between wild-type and CRH KO mice, arguing against compensatory changes in IL-6 responses to restraint due to CRH deficiency. CRH infusion enhanced adrenocortical responses to restraint independently of effects on basal corticosterone levels, suggesting that pituitary-adrenal activity is augmented by factors besides CRH during stress. We conclude that although stress-induced pituitary-adrenal activity does not require acute increases in CRH, CRH is required to support the normal amplitude of adrenocortical axis responsiveness to other endocrine or neural factors during stress.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0028-3835
pubmed:author
pubmed:copyrightInfo
Copyright 2000 S. Karger AG, Basel
pubmed:issnType
Print
pubmed:volume
71
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
79-87
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:10686522-Adrenocorticotropic Hormone, pubmed-meshheading:10686522-Animals, pubmed-meshheading:10686522-Blood Glucose, pubmed-meshheading:10686522-Corticosterone, pubmed-meshheading:10686522-Corticotropin-Releasing Hormone, pubmed-meshheading:10686522-Epinephrine, pubmed-meshheading:10686522-Fasting, pubmed-meshheading:10686522-Female, pubmed-meshheading:10686522-Hypoglycemia, pubmed-meshheading:10686522-Hypoglycemic Agents, pubmed-meshheading:10686522-Hypovolemia, pubmed-meshheading:10686522-Insulin, pubmed-meshheading:10686522-Interleukin-6, pubmed-meshheading:10686522-Male, pubmed-meshheading:10686522-Mice, pubmed-meshheading:10686522-Mice, Inbred C57BL, pubmed-meshheading:10686522-Mice, Knockout, pubmed-meshheading:10686522-Pituitary-Adrenal System, pubmed-meshheading:10686522-Recombinant Proteins, pubmed-meshheading:10686522-Stress, Physiological
pubmed:year
2000
pubmed:articleTitle
CRH deficiency impairs but does not block pituitary-adrenal responses to diverse stressors.
pubmed:affiliation
Division of Endocrinology, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't