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rdf:type |
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lifeskim:mentions |
umls-concept:C0003009,
umls-concept:C0017262,
umls-concept:C0027051,
umls-concept:C0033684,
umls-concept:C0063592,
umls-concept:C0126174,
umls-concept:C0185117,
umls-concept:C0257694,
umls-concept:C0332206,
umls-concept:C0332307,
umls-concept:C0390423,
umls-concept:C0597360,
umls-concept:C1280500,
umls-concept:C1280551,
umls-concept:C1314939,
umls-concept:C1412113,
umls-concept:C1879547,
umls-concept:C2261578,
umls-concept:C2911684
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pubmed:issue |
2
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pubmed:dateCreated |
2002-4-22
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pubmed:abstractText |
To determine whether cardioprotection after chronic angiotensin II (Ang II) type 1 (AT(1)) receptor blockade involves Ang II type 2 (AT(2)) receptor expression and protein kinase C-epsilon (PKC(epsilon)) activation, we measured in vivo haemodynamics and left ventricular (LV) remodelling and dysfunction (echocardiogram/ Doppler) and ex vivo AT(1)/AT(2)-receptor expression, IP(3)R (1, 4, 5-inositol trisphosphate type 2 receptor) and PKC(epsilon) proteins in dogs with acutely reperfused (90 minutes ischaemia, 90 minutes reperfusion) myocardial infarction (MI) following seven days of AT(1)-receptor blockade with oral losartan or UP269-6. The animals were randomised to sham; sham + losartan or UP269-6; MI alone; MI + losartan; MI + UP269-6. More marked AT(1)-receptor blockade with UP269-6 (greater inhibition of Ang II pressor responses) was associated with a smaller increase in preload, less systolic and diastolic dysfunction, less infarct expansion, and smaller LV diastolic and systolic volumes. However, both AT(1)-receptor antagonists decreased infarct size. Importantly, MI decreased AT(1)-receptor and AT(2)-receptor expression while MI after AT(1)-receptor antagonism increased AT(1)-receptor (mRNA, not protein) and AT(2)-receptor (mRNA and protein) expression as well as IP(3)R and PKC(epsilon) proteins and cyclic guanosine 3', 5' monophosphate (cGMP). These results suggest that cardioprotection induced by chronic AT(1)-receptor antagonism involves enhanced AT(2)-receptor expression and possibly downstream signalling through IP(3)R, PKC(epsilon) and cGMP.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin Receptor Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Cardiotonic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic GMP,
http://linkedlifedata.com/resource/pubmed/chemical/Inositol 1,4,5-Trisphosphate...,
http://linkedlifedata.com/resource/pubmed/chemical/Isoenzymes,
http://linkedlifedata.com/resource/pubmed/chemical/Losartan,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C-epsilon,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrimidines,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Angiotensin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytoplasmic and Nuclear,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrazoles,
http://linkedlifedata.com/resource/pubmed/chemical/UP 269-6
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1470-3203
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
184-95
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:11967812-Angiotensin Receptor Antagonists,
pubmed-meshheading:11967812-Animals,
pubmed-meshheading:11967812-Blood Volume,
pubmed-meshheading:11967812-Calcium Channels,
pubmed-meshheading:11967812-Cardiotonic Agents,
pubmed-meshheading:11967812-Cyclic GMP,
pubmed-meshheading:11967812-Dogs,
pubmed-meshheading:11967812-Enzyme Activation,
pubmed-meshheading:11967812-Female,
pubmed-meshheading:11967812-Hemodynamics,
pubmed-meshheading:11967812-Inositol 1,4,5-Trisphosphate Receptors,
pubmed-meshheading:11967812-Isoenzymes,
pubmed-meshheading:11967812-Losartan,
pubmed-meshheading:11967812-Male,
pubmed-meshheading:11967812-Myocardial Infarction,
pubmed-meshheading:11967812-Myocardial Reperfusion,
pubmed-meshheading:11967812-Myocardium,
pubmed-meshheading:11967812-Protein Kinase C,
pubmed-meshheading:11967812-Protein Kinase C-epsilon,
pubmed-meshheading:11967812-Pyrimidines,
pubmed-meshheading:11967812-RNA, Messenger,
pubmed-meshheading:11967812-Receptor, Angiotensin, Type 1,
pubmed-meshheading:11967812-Receptor, Angiotensin, Type 2,
pubmed-meshheading:11967812-Receptors, Angiotensin,
pubmed-meshheading:11967812-Receptors, Cytoplasmic and Nuclear,
pubmed-meshheading:11967812-Tetrazoles,
pubmed-meshheading:11967812-Time Factors,
pubmed-meshheading:11967812-Ventricular Function, Left
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pubmed:year |
2000
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pubmed:articleTitle |
Cardioprotection after angiotensin II type 1 blockade involves angiotensin II type 2 receptor expression and activation of protein kinase C-epsilon in acutely reperfused myocardial infarction in the dog. Effect of UP269-6 and losartan on AT1 and AT2-receptor expression and IP3 receptor and PKCepsilon proteins.
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pubmed:affiliation |
Department of Medicine and the Cardiovascular Research Group, University of Alberta, Edmonton, Alberta, T6G 2R7, Canada.
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pubmed:publicationType |
Journal Article
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