Linked Life Data

17664390

Source:http://linkedlifedata.com/resource/pubmed/id/17664390

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-8-23
pubmed:abstractText
Endothelin (ET) exerts powerful pressor actions primarily through activation of the ET(A) receptor subtype. The ET(B) receptor (ET(B)R) subtype, on the other hand, is generally thought to initiate physiological actions that decrease arterial pressure. Such actions include clearing ET from the bloodstream, initiating endothelium-mediated vasodilation, and facilitating renal sodium and water excretion. The effect of long-term activation of the ET(B)R on arterial pressure, however, never has been directly tested. In this study we evaluated cardiovascular responses to chronic (5-day) activation of ET(B)R in male rats using continuous intravenous infusion of the selective agonist sarafotoxin 6c. Surprisingly, we found that sarafotoxin 6c caused a sustained increase in arterial pressure that rapidly reversed on termination of infusion. The hypertension was associated with increased renal excretion of sodium and water and decreased plasma volume. Alterations in daily sodium intake did not affect the magnitude of the hypertension. Hemodynamic studies revealed a decreased cardiac output and increased total peripheral resistance during sarafotoxin 6c infusion. Infusion of sarafotoxin 6c caused a small increase in plasma ET levels. Nevertheless, the hypertension was not affected by coadministration of a selective ET(A) receptor antagonist (atrasentan) but was completely prevented by treatment with a combined ET(A) receptor and ET(B)R antagonist (A186280). These experiments reveal for the first time that chronic activation of ET(B)R in rats causes sustained hypertension.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
50
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
512-8
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed-meshheading:17664390-Animals, pubmed-meshheading:17664390-Blood Pressure, pubmed-meshheading:17664390-Blood Volume, pubmed-meshheading:17664390-Cardiac Output, pubmed-meshheading:17664390-Disease Models, Animal, pubmed-meshheading:17664390-Diuresis, pubmed-meshheading:17664390-Drug Administration Schedule, pubmed-meshheading:17664390-Endothelin-1, pubmed-meshheading:17664390-Heart Rate, pubmed-meshheading:17664390-Hypertension, pubmed-meshheading:17664390-Male, pubmed-meshheading:17664390-Natriuresis, pubmed-meshheading:17664390-Pyrrolidines, pubmed-meshheading:17664390-Rats, pubmed-meshheading:17664390-Rats, Sprague-Dawley, pubmed-meshheading:17664390-Receptor, Endothelin A, pubmed-meshheading:17664390-Receptor, Endothelin B, pubmed-meshheading:17664390-Stroke Volume, pubmed-meshheading:17664390-Sulfonamides, pubmed-meshheading:17664390-Vascular Resistance, pubmed-meshheading:17664390-Viper Venoms
pubmed:year
2007
pubmed:articleTitle
Chronic activation of endothelin B receptors: new model of experimental hypertension.
pubmed:affiliation
Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824, USA. finkg@msu.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural