Source:http://linkedlifedata.com/resource/pubmed/id/12637351
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2003-6-9
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pubmed:abstractText |
To investigate whether altered function of adenosine receptors could contribute to sinus node or atrioventricular (AV) nodal dysfunction in conscious mammals, we studied transgenic (TG) mice with cardiac-specific overexpression of the A1 adenosine receptor (A1AR). A Holter ECG was recorded in seven freely moving littermate pairs of mice during normal activity, exercise (5 min of swimming), and 1 h after exercise. TG mice had lower maximal heart rates (HR) than wild-type (WT) mice (normal activity: 437 +/- 18 vs. 522 +/- 24 beats/min, P < 0.05; exercise: 650 +/- 13 vs. 765 +/- 28 beats/min, P < 0.05; 1 h after exercise: 588 +/- 18 vs. 720 +/- 12 beats/min, P < 0.05; all values are means +/- SE). Mean HR was lower during exercise (589 +/- 16 vs. 698 +/- 34 beats/min, P < 0.05) and after exercise (495 +/- 16 vs. 592 +/- 27 beats/min, P < 0.05). Minimal HR was not different between genotypes. HR variability (SD of RR intervals) was reduced by 30% (P < 0.05) in TG compared with WT mice. Pertussis toxin (n = 4 pairs, 150 microg/kg ip) reversed bradycardia after 48 h. TG mice showed first-degree AV nodal block (PQ interval: 42 +/- 2 vs. 37 +/- 2 ms, P < 0.05), which was diminished but not abolished by pertussis toxin. Isolated Langendorff-perfused TG hearts developed spontaneous atrial arrhythmias (3 of 6 TG mice vs. 0 of 9 WT mice, P < 0.05). In conclusion, A1AR regulate sinus nodal and AV nodal function in the mammalian heart in vivo. Enhanced expression of A1AR causes sinus nodal and AV nodal dysfunction and supraventricular arrhythmias.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0363-6135
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pubmed:author |
pubmed-author:BabaHideo AHA,
pubmed-author:BoknikPeterP,
pubmed-author:BreithardtGunterG,
pubmed-author:FabritzLarissaL,
pubmed-author:FortmullerLisaL,
pubmed-author:KirchhofPaulusP,
pubmed-author:LankfordAmyA,
pubmed-author:MatherneG PaulGP,
pubmed-author:NeumannJoachimJ,
pubmed-author:SchmitzWilhelmW
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pubmed:issnType |
Print
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pubmed:volume |
285
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H145-53
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12637351-Animals,
pubmed-meshheading:12637351-Atrioventricular Node,
pubmed-meshheading:12637351-Cardiac Pacing, Artificial,
pubmed-meshheading:12637351-Echocardiography, Doppler,
pubmed-meshheading:12637351-Electrocardiography,
pubmed-meshheading:12637351-Heart Rate,
pubmed-meshheading:12637351-Mice,
pubmed-meshheading:12637351-Mice, Transgenic,
pubmed-meshheading:12637351-Muscle Proteins,
pubmed-meshheading:12637351-Myocardium,
pubmed-meshheading:12637351-Pertussis Toxin,
pubmed-meshheading:12637351-Receptors, Purinergic P1,
pubmed-meshheading:12637351-Sinoatrial Node,
pubmed-meshheading:12637351-Telemetry
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pubmed:year |
2003
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pubmed:articleTitle |
Altered sinus nodal and atrioventricular nodal function in freely moving mice overexpressing the A1 adenosine receptor.
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pubmed:affiliation |
Department of Cardiology and Angiology, University Hospital Münster, D-48129 Münster, Germany. kirchhp@uni-muenster.de
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pubmed:publicationType |
Journal Article,
In Vitro
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