Linked Life Data

2546748

Source:http://linkedlifedata.com/resource/pubmed/id/2546748

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1989-8-29
pubmed:abstractText
The effects of naloxone, an opioid antagonist, on arginine vasopressin (AVP) secretion were examined in conscious unrestrained rats under both basal and stimulated conditions. Intravenous injection of naloxone in a dose of 0.1 mg/kg did not significantly affect the basal plasma AVP level. However, 0.5 or 2.5 mg/kg naloxone significantly raised the basal AVP level in euhydrated rats. Naloxone (0.5 mg/kg) significantly enhanced AVP secretion after 72-h water deprivation. However, the enhancement was more prominent in euhydrated rats than in dehydrated rats. Pretreatment with naloxone (0.5 mg/kg) also significantly prolonged AVP secretion induced by intracerebroventricular injection of angiotensin-II (100 ng). Moreover, naloxone (0.5 mg/kg) significantly increased AVP secretion induced by intracerebroventricular injection of carbachol (10 ng). Naloxone (0.5 mg/kg) altered neither basal blood pressure nor the angiotensin-II-induced pressor response, but augmented the carbachol-induced pressor response. This suggests that facilitation of AVP secretion by naloxone is not due to a reflex mechanism resulting from decreased blood pressure. These results indicate that endogenous opioid peptides exert a tonic inhibitory control on AVP secretion in rats.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
125
pubmed:owner
NLM
pubmed:authorsComplete
N
pubmed:pagination
785-90
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Effects of naloxone on vasopressin secretion in conscious rats: evidence for inhibitory role of endogenous opioid peptides in vasopressin secretion.
pubmed:affiliation
Department of Medicine, Kyoto University School of Medicine, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't