Linked Life Data

11434508

Source:http://linkedlifedata.com/resource/pubmed/id/11434508

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2001-7-3
pubmed:abstractText
Vascular responses to acetylcholine (ACh) are notoriously variable, the reason for this phenomenon is unknown. We tested the hypothesis that the variability in venous response to acetylcholine may be associated with two recently identified genetic polymorphisms for proteins involved in the signal transduction pathway, i.e. the G-protein beta3-subunit (GNB3) and endothelial nitric oxide synthase (eNOS). The dorsal hand vein technique was used in 37 healthy subjects. Hand veins were preconstricted with the alpha1-adrenoceptor agonist phenylephrine and the venodilator response to local ACh infusion was measured with and without comedication of acetylsalicylic acid or co-infusion of N(G)-monomethyl-L-arginine (L-NMMA). In addition, all subjects received routine laboratory tests and 26 of them were genotyped for the C825T polymorphism of the GNB3 gene and for the G894T polymorphism of the eNOS gene. A striking variability in venous response to ACh was found with dilation observed in the low ACh concentration range and reduced dilation or even constriction at high concentrations. ACh-induced venodilation was mediated by muscarinic receptors and abolished in the presence of both acetylsalicylic acid and L-NMMA suggesting dependence on endothelium. We did not find any association of the variability in ACh response with GNB3 or eNOS allele status. On the other hand, a significant positive correlation between ACh responsiveness and low density lipoprotein-cholesterol status was detected. Two recently discovered gene polymorphisms are not responsible for the profound heterogeneity in venodilator response to ACh. Surprisingly, this variability appears to relate to the lipid status of the subjects. The exact nature of this new finding requires further study.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0960-314X
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
307-16
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11434508-Acetylcholine, pubmed-meshheading:11434508-Adult, pubmed-meshheading:11434508-Aspirin, pubmed-meshheading:11434508-Cholesterol, LDL, pubmed-meshheading:11434508-Endothelium, Vascular, pubmed-meshheading:11434508-Female, pubmed-meshheading:11434508-Genotype, pubmed-meshheading:11434508-Hand, pubmed-meshheading:11434508-Heterotrimeric GTP-Binding Proteins, pubmed-meshheading:11434508-Humans, pubmed-meshheading:11434508-Male, pubmed-meshheading:11434508-Models, Cardiovascular, pubmed-meshheading:11434508-Nitric Oxide Synthase, pubmed-meshheading:11434508-Nitric Oxide Synthase Type III, pubmed-meshheading:11434508-Polymorphism, Genetic, pubmed-meshheading:11434508-Receptors, Muscarinic, pubmed-meshheading:11434508-Triglycerides, pubmed-meshheading:11434508-Vasodilation, pubmed-meshheading:11434508-Veins, pubmed-meshheading:11434508-omega-N-Methylarginine
pubmed:year
2001
pubmed:articleTitle
Heterogeneity in hand veins responses to acetylcholine is not associated with polymorphisms in the G-protein beta3-subunit (C825T) and endothelial nitric oxide synthase (G894T) genes but with serum low density lipoprotein cholesterol.
pubmed:affiliation
Institute of Clinical Pharmacology, Medical Faculty of the University of Technology Dresden, Germany. grossmann@ikp.de
pubmed:publicationType
Journal Article