Linked Life Data

14732736

Source:http://linkedlifedata.com/resource/pubmed/id/14732736

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-1-30
pubmed:abstractText
We have previously shown that a decrease in hypothalamic gamma adducin (gamma-adducin) is associated with hypertension in the spontaneously hypertensive rat (SHR). In view of many inherent issues with SHR, our objective in the present study was to provide proof of this concept with the use of 2 nongenetic rat models of hypertension. Subcutaneous angiotensin II (Ang II) infusion for 2 weeks (55 ng/kg per day) resulted in an increase in blood pressure (BP) of 18 mm Hg. This was associated with a 70% decrease in hypothalamic gamma-adducin. Concomitant administration of losartan attenuated the development of hypertension and a decrease in gamma-adducin. Deoxycorticosterone acetate salt-induced hypertension also caused a 70% decrease in hypothalamic gamma-adducin. Finally, neuronal cultures from neonatal rat brains were incubated with 100 nmol/L Ang II for 4 hours to mimic the in vivo Ang II infusion rat model. This chronic incubation with Ang II resulted in a 60% decrease in the neuronal gamma-adducin. Taken together, these observations strengthen our hypothesis that a decrease in hypothalamic gamma-adducin is linked to hypertension.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
43
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
324-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Decrease in hypothalamic gamma adducin in rat models of hypertension.
pubmed:affiliation
Department of Physiology and Functional Genomics, University of Florida McKnight Brain Institute, Gainesville, FL 32610, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.