Linked Life Data

9214448

Source:http://linkedlifedata.com/resource/pubmed/id/9214448

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1997-8-7
pubmed:abstractText
Portal hypertension (PHT) is characterized by splanchnic hyperemia due to a reduction in mesenteric vascular resistance. The reasons for the decreased resistance include an increased responsiveness to a vasodilator substance. Because the activation of an inhibitory guanine nucleotide regulatory (Gi) protein can result in endothelium-dependent relaxation, we tested the hypothesis that exaggerated Gi-protein induced relaxation via a nitric oxide (NO)-dependent pathway partly reflects the enhanced Gi-protein expression in PHT vessels. PHT was created in Sprague-Dawley rats by a partial portal-vein ligation. Control animals were sham operated. Using isolated vascular rings in the absence or presence of an intact endothelium, N(G)-nitro-L-arginine methyl ester (L-NAME), and pertussis toxin, dose response relationships for sodium fluoride (NaF; range, 0.1-4 mmol/L), a Gi protein activator, were determined in a cumulative manner. Gi-protein expression was determined by Western blotting. NaF caused a dose-dependent relaxation in both sham and portal hypertensive pre-contracted vessels, an effect that was significantly inhibited by pertussis toxin, endothelial denudation, and L-NAME. Concentrations of NaF greater than 4 mmol/L caused contractions, an effect that was unaffected by L-NAME. The NaF-induced relaxation response was significantly greater in PHT vessels as compared with sham concomitant with increased Gi-protein expression in PHT vessels. These data suggest that the enhanced endothelial Gi-protein-induced relaxation in PHT vessels may partly reflect enhanced expression of Gi-proteins in PHT vessels and may, thus, represent an important mechanism for exaggerated NO-dependent relaxation in the PHT vasculature.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0270-9139
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
27-33
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:9214448-Animals, pubmed-meshheading:9214448-Blotting, Western, pubmed-meshheading:9214448-Dose-Response Relationship, Drug, pubmed-meshheading:9214448-Endothelium, Vascular, pubmed-meshheading:9214448-Enzyme Inhibitors, pubmed-meshheading:9214448-GTP-Binding Protein alpha Subunits, Gi-Go, pubmed-meshheading:9214448-GTP-Binding Protein alpha Subunits, Gs, pubmed-meshheading:9214448-Hemodynamics, pubmed-meshheading:9214448-Hypertension, Portal, pubmed-meshheading:9214448-Male, pubmed-meshheading:9214448-Methoxamine, pubmed-meshheading:9214448-Muscle Contraction, pubmed-meshheading:9214448-Muscle Relaxation, pubmed-meshheading:9214448-NG-Nitroarginine Methyl Ester, pubmed-meshheading:9214448-Nitric Oxide, pubmed-meshheading:9214448-Nitric Oxide Synthase, pubmed-meshheading:9214448-Potassium Chloride, pubmed-meshheading:9214448-Rats, pubmed-meshheading:9214448-Rats, Sprague-Dawley, pubmed-meshheading:9214448-Sodium Fluoride
pubmed:year
1997
pubmed:articleTitle
Enhanced G-protein-induced relaxation in portal hypertensive rats: role of nitric oxide.
pubmed:affiliation
Department of Surgery, Georgetown University Medical Center, Washington, DC 20007, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't