| pubmed-article:19424280 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19424280 | lifeskim:mentions | umls-concept:C0016059 | lld:lifeskim |
| pubmed-article:19424280 | lifeskim:mentions | umls-concept:C1882687 | lld:lifeskim |
| pubmed-article:19424280 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:19424280 | lifeskim:mentions | umls-concept:C1097411 | lld:lifeskim |
| pubmed-article:19424280 | lifeskim:mentions | umls-concept:C1948023 | lld:lifeskim |
| pubmed-article:19424280 | lifeskim:mentions | umls-concept:C0205464 | lld:lifeskim |
| pubmed-article:19424280 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:19424280 | pubmed:dateCreated | 2009-7-6 | lld:pubmed |
| pubmed-article:19424280 | pubmed:abstractText | Cardiac fibrosis is a hallmark of cardiovascular remodeling associated with hypertension. The purpose of this study was to explore the effect and mechanism of soluble guanylate cyclase (sGC) stimulator BAY 41-2272, leading to intracellular cyclic guanosine monophosphate (cGMP) elevation, on the remodeling process induced by pressure overload. Seven-week-old male Wistar rats with hypertension induced by suprarenal aortic constriction (AC) were treated orally with 2 mg kg(-1) day(-1) of BAY 41-2272 for 14 days. BAY 41-2272 had no effects on blood pressure, but decreased AC-induced collagen accumulation in the left ventricle (LV), inhibiting the number of myofibroblasts and gene expressions of transforming growth factor-beta1 and type 1 collagen. In addition, the antifibrotic action of BAY 41-2272 was accompanied by reducing AC-induced angiotensin-converting enzyme (ACE) mRNA and its enzymatic activity, and angiotensin II concentration in LV. In cultured cardiac fibroblasts, BAY 41-2272 inhibited ACE synthesis and myofibroblast transformation, accompanied by elevating the intracellular cGMP concentration. These results suggest that sGC stimulator BAY 41-2272 might be effective to reduce fibrosis in hypertensive heart disease by attenuating angiotensin II generation through myofibroblast transformation. | lld:pubmed |
| pubmed-article:19424280 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19424280 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19424280 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19424280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19424280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19424280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19424280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19424280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19424280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19424280 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19424280 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19424280 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:19424280 | pubmed:issn | 1348-4214 | lld:pubmed |
| pubmed-article:19424280 | pubmed:author | pubmed-author:KitamuraKazuo... | lld:pubmed |
| pubmed-article:19424280 | pubmed:author | pubmed-author:StaschJohanne... | lld:pubmed |
| pubmed-article:19424280 | pubmed:author | pubmed-author:TsurudaToshih... | lld:pubmed |
| pubmed-article:19424280 | pubmed:author | pubmed-author:HatakeyamaKin... | lld:pubmed |
| pubmed-article:19424280 | pubmed:author | pubmed-author:AsadaYujiroY | lld:pubmed |
| pubmed-article:19424280 | pubmed:author | pubmed-author:ImamuraTakuro... | lld:pubmed |
| pubmed-article:19424280 | pubmed:author | pubmed-author:KatoJohjiJ | lld:pubmed |
| pubmed-article:19424280 | pubmed:author | pubmed-author:MasuyamaHiroy... | lld:pubmed |
| pubmed-article:19424280 | pubmed:author | pubmed-author:SekitaYokoY | lld:pubmed |
| pubmed-article:19424280 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19424280 | pubmed:volume | 32 | lld:pubmed |
| pubmed-article:19424280 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19424280 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19424280 | pubmed:pagination | 597-603 | lld:pubmed |
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| pubmed-article:19424280 | pubmed:meshHeading | pubmed-meshheading:19424280... | lld:pubmed |
| pubmed-article:19424280 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19424280 | pubmed:articleTitle | Pressure-independent effects of pharmacological stimulation of soluble guanylate cyclase on fibrosis in pressure-overloaded rat heart. | lld:pubmed |
| pubmed-article:19424280 | pubmed:affiliation | Department of Internal Medicine, Circulatory and Body Fluid Regulation, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan. | lld:pubmed |
| pubmed-article:19424280 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19424280 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
