Linked Life Data

2331601

Source:http://linkedlifedata.com/resource/pubmed/id/2331601

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1990-6-4
pubmed:abstractText
Angiotensinergic synapses in the central nervous system (CNS) have been proposed to be involved in drinking induced by both intracerebroventricular (i.c.v.) and peripheral administration of angiotensins. In the present studies, we tested this hypothesis with i.c.v. application of amastatin, an aminopeptidase A inhibitor, to block peptide degradation. Potentiation of i.c.v. angiotensin II (Ang II)-induced drinking responses was observed when amastatin and Ang II were administered. Amastatin did not potentiate drinking to carbachol which demonstrates that the enhancement is specific to peptides. Centrally administered amastatin also potentiated drinking following systemic administration of Asn1 angiotensin II. (Asn1 Ang II). The results are consistent with the hypothesis that CNS angiotensin synapses are involved in the dipsogenic response that results from elevated levels of circulating angiotensin.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
510
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
237-41
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Amastatin potentiation of drinking induced by blood-borne angiotensin: evidence for mediation by endogenous brain angiotensin.
pubmed:affiliation
Department of Psychology, University of Iowa, Iowa City 52242.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't