Linked Life Data

8453478

Source:http://linkedlifedata.com/resource/pubmed/id/8453478

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1993-4-16
pubmed:abstractText
Intracerebroventricular (i.c.v.) angiotensin II (ANG II) increases vascular resistance and elicits a pressor response characterized by sympathetic nervous system activation (SNS component) and increased vasopressin (VP) secretion (VP component). This study examines the role of brain AT1 and AT2 ANG II receptors in mediating the pressor and renal hemodynamic effects of i.c.v. ANG II in conscious Sprague-Dawley rats. Mean arterial pressure, heart rate and renal vascular resistance responses to i.c.v. ANG II (100 ng in 5 microliters) were determined 10 min after i.c.v. injection of either the AT1 receptor antagonist, DuP 753 (1.0, 2.5, 5.0, 10.0 micrograms), the AT2 receptor ligand, PD 123319 (3.5 x [10(-6), 10(-4), 10(-2), 10(0)] micrograms), or both. In control rats, i.c.v. DuP 753 prevented the pressor response and the increase in renal vascular resistance that occurred following i.c.v. ANG II in a dose-dependent manner (P < 0.05), while i.c.v. PD 123319 was without affect. When the VP- and SNS components were studied individually, by preventing the SNS component with intravenous (i.v.) chlorisondamine or the VP component with a V1 receptor antagonist (i.v.) similar results were obtained; DuP 753 prevented the SNS component and significantly reduced the VP component. These results indicate that both central ANG II pressor components are mediated primarily by brain AT1 receptors. However, doses of DuP 753 were more effective when combined with 3.5 micrograms of PD 123319 than when given alone (P < 0.05), suggesting that the pressor effects of i.c.v. ANG II may involve activation of multiple ANG II receptor subtypes.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
12
pubmed:volume
603
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
57-63
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:8453478-Angiotensin I, pubmed-meshheading:8453478-Angiotensin II, pubmed-meshheading:8453478-Angiotensin Receptor Antagonists, pubmed-meshheading:8453478-Animals, pubmed-meshheading:8453478-Biphenyl Compounds, pubmed-meshheading:8453478-Blood Pressure, pubmed-meshheading:8453478-Brain, pubmed-meshheading:8453478-Chlorisondamine, pubmed-meshheading:8453478-Dose-Response Relationship, Drug, pubmed-meshheading:8453478-Heart Rate, pubmed-meshheading:8453478-Imidazoles, pubmed-meshheading:8453478-Injections, Intraventricular, pubmed-meshheading:8453478-Losartan, pubmed-meshheading:8453478-Male, pubmed-meshheading:8453478-Pyridines, pubmed-meshheading:8453478-Rats, pubmed-meshheading:8453478-Rats, Sprague-Dawley, pubmed-meshheading:8453478-Receptors, Angiotensin, pubmed-meshheading:8453478-Renal Circulation, pubmed-meshheading:8453478-Tetrazoles
pubmed:year
1993
pubmed:articleTitle
Functional role of brain AT1 and AT2 receptors in the central angiotensin II pressor response.
pubmed:affiliation
Department of Pharmacology, University of Texas Health Science Center, San Antonio 78282-7764.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't