|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
3
|
|
pubmed:dateCreated |
2010-5-13
|
|
pubmed:abstractText |
alpha(2)-Adrenoceptors modulate cardiovascular function by vasoconstriction or dilatation, by central inhibition of sympathetic activity, or by feedback inhibition of norepinephrine release from sympathetic neurons. Despite detailed knowledge about subtype-specific functions of alpha(2)-receptors, the relative contributions of sympathetic vs. non-sympathetic receptors involved in these cardiovascular effects have not been identified. The aim of this study was to define the physiological and pharmacological role of alpha(2A)-adrenoceptors in adrenergic vs. non-adrenergic cells at baseline and during sympathetic stress.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/ADRA2A protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/ADRA2C protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Adra2a protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Adra2c protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic alpha-Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Dopamine beta-Hydroxylase,
http://linkedlifedata.com/resource/pubmed/chemical/Medetomidine,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, alpha-2
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Jun
|
|
pubmed:issn |
1755-3245
|
|
pubmed:author |
|
|
pubmed:issnType |
Electronic
|
|
pubmed:day |
1
|
|
pubmed:volume |
86
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
432-42
|
|
pubmed:dateRevised |
2010-11-18
|
|
pubmed:meshHeading |
pubmed-meshheading:20083574-Adrenergic alpha-Agonists,
pubmed-meshheading:20083574-Animals,
pubmed-meshheading:20083574-Blood Pressure,
pubmed-meshheading:20083574-Cardiomegaly,
pubmed-meshheading:20083574-Cells, Cultured,
pubmed-meshheading:20083574-Disease Models, Animal,
pubmed-meshheading:20083574-Dopamine beta-Hydroxylase,
pubmed-meshheading:20083574-Dose-Response Relationship, Drug,
pubmed-meshheading:20083574-Endocytosis,
pubmed-meshheading:20083574-Feedback, Physiological,
pubmed-meshheading:20083574-Fibrosis,
pubmed-meshheading:20083574-Gene Expression Profiling,
pubmed-meshheading:20083574-Heart,
pubmed-meshheading:20083574-Heart Rate,
pubmed-meshheading:20083574-Humans,
pubmed-meshheading:20083574-Hypertension,
pubmed-meshheading:20083574-Medetomidine,
pubmed-meshheading:20083574-Mice,
pubmed-meshheading:20083574-Mice, Inbred C57BL,
pubmed-meshheading:20083574-Mice, Knockout,
pubmed-meshheading:20083574-Mice, Transgenic,
pubmed-meshheading:20083574-Myocardium,
pubmed-meshheading:20083574-Neurites,
pubmed-meshheading:20083574-Norepinephrine,
pubmed-meshheading:20083574-Promoter Regions, Genetic,
pubmed-meshheading:20083574-RNA, Messenger,
pubmed-meshheading:20083574-Receptors, Adrenergic, alpha-2,
pubmed-meshheading:20083574-Sympathetic Fibers, Postganglionic,
pubmed-meshheading:20083574-Sympathetic Nervous System
|
|
pubmed:year |
2010
|
|
pubmed:articleTitle |
Sympathetic alpha(2)-adrenoceptors prevent cardiac hypertrophy and fibrosis in mice at baseline but not after chronic pressure overload.
|
|
pubmed:affiliation |
Institute of Experimental and Clinical Pharmacology and Toxicology, University of Freiburg, Albertstrasse 25, Freiburg 79104, Germany.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
