| pubmed-article:11927520 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11927520 | lifeskim:mentions | umls-concept:C0018801 | lld:lifeskim |
| pubmed-article:11927520 | lifeskim:mentions | umls-concept:C0027051 | lld:lifeskim |
| pubmed-article:11927520 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:11927520 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
| pubmed-article:11927520 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:11927520 | lifeskim:mentions | umls-concept:C0103306 | lld:lifeskim |
| pubmed-article:11927520 | pubmed:issue | 13 | lld:pubmed |
| pubmed-article:11927520 | pubmed:dateCreated | 2002-4-2 | lld:pubmed |
| pubmed-article:11927520 | pubmed:abstractText | The renin-angiotensin system (RAS) is a key player in the progression of heart failure. Angiotensin-(1-7) is thought to modulate the activity of the RAS. Furthermore, this peptide may play a part in the beneficial effects of angiotensin-converting enzyme inhibitors in cardiovascular disease. We assessed the effects of angiotensin-(1-7) on the progression of heart failure. | lld:pubmed |
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| pubmed-article:11927520 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11927520 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11927520 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:11927520 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11927520 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:11927520 | pubmed:issn | 1524-4539 | lld:pubmed |
| pubmed-article:11927520 | pubmed:author | pubmed-author:TioRené ARA | lld:pubmed |
| pubmed-article:11927520 | pubmed:author | pubmed-author:van... | lld:pubmed |
| pubmed-article:11927520 | pubmed:author | pubmed-author:HenningRobert... | lld:pubmed |
| pubmed-article:11927520 | pubmed:author | pubmed-author:SuurmeijerAlb... | lld:pubmed |
| pubmed-article:11927520 | pubmed:author | pubmed-author:RoksAnton J... | lld:pubmed |
| pubmed-article:11927520 | pubmed:author | pubmed-author:LootAnnemarie... | lld:pubmed |
| pubmed-article:11927520 | pubmed:author | pubmed-author:BoomsmaFransF | lld:pubmed |
| pubmed-article:11927520 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:11927520 | pubmed:day | 2 | lld:pubmed |
| pubmed-article:11927520 | pubmed:volume | 105 | lld:pubmed |
| pubmed-article:11927520 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11927520 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11927520 | pubmed:pagination | 1548-50 | lld:pubmed |
| pubmed-article:11927520 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:11927520 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11927520 | pubmed:articleTitle | Angiotensin-(1-7) attenuates the development of heart failure after myocardial infarction in rats. | lld:pubmed |
| pubmed-article:11927520 | pubmed:affiliation | Department of Clinical Pharmacology, University of Groningen, The Netherlands. a.e.loot@med.rug.nl | lld:pubmed |
| pubmed-article:11927520 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11927520 | pubmed:publicationType | In Vitro | lld:pubmed |
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