Linked Life Data

12519093

Source:http://linkedlifedata.com/resource/pubmed/id/12519093

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2003-4-17
pubmed:abstractText
Common naturally occurring polymorphisms have been identified in the coding regions of the alpha(1A)-, alpha(2B)-, beta(1)- and beta(2)-adrenoceptor (AR) genes [alpha(1A)-AR R492C, alpha(2B)-AR insertion/deletion (I/D), beta(1)-AR R389G, beta(2)-AR G16R and beta(2)-AR Q27E] and are associated with modified in vivo and in vitro functionality. We tested their possible effects on the haemodynamic responses to intravenous adrenaline (20, 40, 80 and 160 ng/kg of body weight per min; 5 min for each infusion rate) before and after beta-blockade (propranolol) in 16 young healthy men. We monitored changes in heart rate, blood pressure (BP), ECG, coronary flow velocity and plasma adrenaline and noradrenaline. The Cys/Cys (CC) genotype of the alpha(1A)-AR R492C polymorphism was associated with a longer ECG PR interval before and during the adrenaline infusions. The deletion/deletion (D/D) genotype of the alpha(2B)-AR I/D polymorphism was associated with blunted coronary blood flow increases during the adrenaline infusion before beta-blockade. The beta(1)-AR R389G polymorphism was not associated with modified responses to infused adrenaline. Subjects carrying the Gly/Gly (GG) genotype of the beta(2)-AR G16R polymorphism demonstrated increases in diastolic BP upon adrenaline infusion, whereas diastolic BP was decreased in the other genotype groups. These results suggest that, upon acute adrenaline infusion, the alpha(2B)-AR D/D genotype confers increased vasoconstriction and that the beta(2)-AR GG genotype confers reduced vasodilatation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0143-5221
pubmed:author
pubmed:issnType
Print
pubmed:volume
104
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
509-20
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12519093-Adrenergic beta-Antagonists, pubmed-meshheading:12519093-Adult, pubmed-meshheading:12519093-Blood Flow Velocity, pubmed-meshheading:12519093-Blood Pressure, pubmed-meshheading:12519093-Coronary Circulation, pubmed-meshheading:12519093-Drug Administration Schedule, pubmed-meshheading:12519093-Echocardiography, pubmed-meshheading:12519093-Electrocardiography, pubmed-meshheading:12519093-Epinephrine, pubmed-meshheading:12519093-Genotype, pubmed-meshheading:12519093-Heart Rate, pubmed-meshheading:12519093-Humans, pubmed-meshheading:12519093-Infusions, Intravenous, pubmed-meshheading:12519093-Least-Squares Analysis, pubmed-meshheading:12519093-Male, pubmed-meshheading:12519093-Multivariate Analysis, pubmed-meshheading:12519093-Norepinephrine, pubmed-meshheading:12519093-Polymorphism, Genetic, pubmed-meshheading:12519093-Propranolol, pubmed-meshheading:12519093-Receptors, Adrenergic, pubmed-meshheading:12519093-Receptors, Adrenergic, alpha-1, pubmed-meshheading:12519093-Receptors, Adrenergic, alpha-2, pubmed-meshheading:12519093-Receptors, Adrenergic, beta-1, pubmed-meshheading:12519093-Receptors, Adrenergic, beta-2
pubmed:year
2003
pubmed:articleTitle
Effects of common polymorphisms in the alpha1A-, alpha2B-, beta1- and beta2-adrenoreceptors on haemodynamic responses to adrenaline.
pubmed:affiliation
Department of Pharmacology and Clinical Pharmacology, University of Turku, Itäinen Pitkäkatu 4, Finland. snapir@utu.fi
pubmed:publicationType
Journal Article, Clinical Trial, Research Support, Non-U.S. Gov't