Linked Life Data

15725951

Source:http://linkedlifedata.com/resource/pubmed/id/15725951

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-2-23
pubmed:abstractText
Platelets play a pivotal role in the pathophysiology of acute coronary syndromes. Chronic beta-blockade has been shown to improve the long-term clinical outcome in coronary heart disease. Because platelets play a central role in thrombus formation, the aim of the present study was to investigate if chronic beta-blockade may transregulate the expression of alpha2-adrenergic receptors on human platelets and via this mechanism may modulate platelet activation. The densities of alpha2-adrenergic receptors of platelets were determined in healthy volunteers under chronic beta-blockade and as alpha2-adrenergic receptor-mediated function in catecholamine-induced platelet aggregation was determined. Chronic beta-blockade induced a time-dependent reduction of alpha2-adrenergic receptors. This reduction was accompanied by a decrease of the alpha-subunit of Gi proteins as demonstrated by Western blot analysis. This transregulation at both the receptor level and the G-protein level resulted in an almost complete loss of the alpha2-adrenergic receptor-mediated inhibition of adenylyl cyclase. The impairment of the alpha2-adrenergic receptor system correlated with a reduction of the catecholamine-induced activation and aggregation of human platelets. The functional transregulation of alpha2-adrenergic receptors by chronic beta-blockade in platelets and the consequent impairment of platelet activation may contribute to the therapeutic success of beta-blocker therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
253-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15725951-Adenylate Cyclase, pubmed-meshheading:15725951-Adrenergic alpha-Agonists, pubmed-meshheading:15725951-Adrenergic alpha-Antagonists, pubmed-meshheading:15725951-Adrenergic beta-Antagonists, pubmed-meshheading:15725951-Adult, pubmed-meshheading:15725951-Blood Platelets, pubmed-meshheading:15725951-Cell Membrane, pubmed-meshheading:15725951-Clonidine, pubmed-meshheading:15725951-Electrophoresis, Polyacrylamide Gel, pubmed-meshheading:15725951-Epinephrine, pubmed-meshheading:15725951-GTP-Binding Proteins, pubmed-meshheading:15725951-Humans, pubmed-meshheading:15725951-Immunoblotting, pubmed-meshheading:15725951-Platelet Aggregation, pubmed-meshheading:15725951-Receptors, Adrenergic, alpha-2, pubmed-meshheading:15725951-Signal Transduction, pubmed-meshheading:15725951-Yohimbine
pubmed:year
2005
pubmed:articleTitle
Transregulation of the alpha2-adrenergic signal transduction pathway by chronic beta-blockade: a novel mechanism for decreased platelet aggregation in patients.
pubmed:affiliation
Medical Clinic II, Department of Cardiology, University of Technology Dresden, Dresden, Germany.
pubmed:publicationType
Journal Article, In Vitro