Linked Life Data

18716370

Source:http://linkedlifedata.com/resource/pubmed/id/18716370

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2008-8-21
pubmed:abstractText
Recently we have shown functional involvement of the phosphatidylinositol 3-kinase (PI3K)-Akt-nitric oxide synthase (NOS) signaling pathway in central control of cardiovascular effects in the nucleus tractus solitarii (NTS) of normotensive Wistar-Kyoto (WKY) rats. In this study we determined whether PI3K/Akt signaling was defective in spontaneously hypertensive rats (SHR). WKY rats and SHR were anesthetized with urethane. Mean blood pressure (MBP) and heart rate (HR) were monitored intra-arterially. Unilateral microinjection (60 nL) of insulin (100 IU/mL) into the NTS produced prominent depressor and bradycardic effects in 8- and 16-week-old normotensive WKY and 8-week-old SHR. However, no significant cardiovascular effects were found in 16-week-old SHR after insulin injection. Furthermore, pretreatment with PI3K inhibitor LY294002 and NOS inhibitor L-NAME into the NTS attenuated the cardiovascular response evoked by insulin in WKY and 8-week-old SHR but not in 16-week-old SHR. Unilateral microinjection of 1 mmol/L of PI(3,4,5)P(3) (phosphatidylinositol 3,4,5-triphosphate), a phospholipids second messenger produced by PI3K, into the NTS produced prominent depressor and bradycardic effects in 8- or 16-week-old WKY rats as well as 8-week-old SHR but not in 16-week-old SHR. Western blot analysis showed no significant increase in Akt phosphorylation in 8-week-old pre-hypertensive SHR after insulin injection. Similar results were also found in hypertensive 16-week-old SHR. Our results indicate that the Akt-independent signaling pathway is involved in NOS activation to regulate cardiovascular effects in the NTS of 8-week-old pre-hypertensive SHR. Both Akt-dependent and Akt-independent signaling pathways are defective in hypertensive 16-week-old SHR.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0916-9636
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1209-18
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:18716370-Animals, pubmed-meshheading:18716370-Blood Pressure, pubmed-meshheading:18716370-Chromones, pubmed-meshheading:18716370-Heart Rate, pubmed-meshheading:18716370-Insulin, pubmed-meshheading:18716370-Male, pubmed-meshheading:18716370-Morpholines, pubmed-meshheading:18716370-NG-Nitroarginine Methyl Ester, pubmed-meshheading:18716370-Phosphatidylinositol 3-Kinases, pubmed-meshheading:18716370-Phosphatidylinositol Phosphates, pubmed-meshheading:18716370-Phosphorylation, pubmed-meshheading:18716370-Proto-Oncogene Proteins c-akt, pubmed-meshheading:18716370-Rats, pubmed-meshheading:18716370-Rats, Inbred SHR, pubmed-meshheading:18716370-Rats, Inbred WKY, pubmed-meshheading:18716370-Receptor, Insulin, pubmed-meshheading:18716370-Signal Transduction, pubmed-meshheading:18716370-Solitary Nucleus
pubmed:year
2008
pubmed:articleTitle
Defective phosphatidylinositol 3-kinase signaling in central control of cardiovascular effects in the nucleus tractus solitarii of spontaneously hypertensive rats.
pubmed:affiliation
Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, ROC.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't