Linked Life Data

8024023

Source:http://linkedlifedata.com/resource/pubmed/id/8024023

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6 Pt 2
pubmed:dateCreated
1994-8-2
pubmed:abstractText
Glucocorticoid deficiency leads to elevated plasma vasopressin (AVP), while chronic endogenous hypercortisolism may inhibit osmotically stimulated AVP, suggesting that glucocorticoids may be feedback inhibitors of AVP secretion. We evaluated the effect of physiological increases in cortisol (65 mg/day iv) for 7 days on basal AVP and oxytocin (OT) in five conscious, male dogs. Cortisol increased from 1.3 +/- 0.1 to 5.0 +/- 0.8 micrograms/dl during infusion. Basal plasma AVP significantly decreased from 3.5 +/- 0.2 to 2.6 +/- 0.3 pg/ml during cortisol infusion. Plasma OT, osmolality, and sodium did not change while arterial pressure decreased (from 107 +/- 3 to 102 +/- 2 mmHg) on days 4 and 6. Increases in cortisol led to a physiologically significant, nonosmotic decrease in AVP. The effect was specific to AVP and independent of changes in arterial pressure. Glucocorticoid administration significantly decreased basal AVP within 24 h, which is comparable to the negative feedback control of adrenocorticotropic hormone. The inverse relationship between cortisol and AVP may account for the nonosmotic change in AVP in patients with disorders of glucocorticoid secretion.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
266
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R1744-51
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Physiological increases in cortisol inhibit basal vasopressin release in conscious dogs.
pubmed:affiliation
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.