Abstract | OBJECTIVES: We investigated if endothelin (ET)-1 and the renin-angiotensin-aldosterone system play a role in cardiac fibrosis. BACKGROUND:
Angiotensin II (Ang II) can induce cardiac fibrosis, but the underlying mechanisms are incompletely understood. METHODS: RESULTS: CONCLUSIONS:
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Authors | Teresa M Seccia, Anna S Belloni, Reinhold Kreutz, Martin Paul, Gastone G Nussdorfer, Achille C Pessina, Gian Paolo Rossi |
Journal | Journal of the American College of Cardiology
(J Am Coll Cardiol)
Vol. 41
Issue 4
Pg. 666-73
(Feb 19 2003)
ISSN: 0735-1097 [Print] United States |
PMID | 12598081
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antihypertensive Agents
- Biphenyl Compounds
- Dansyl Compounds
- Endothelin-1
- Receptor, Angiotensin, Type 1
- Receptors, Angiotensin
- Receptors, Cell Surface
- Sulfonamides
- Tetrazoles
- Vasoconstrictor Agents
- Angiotensin II
- 5-(dimethylamino)-N-(3,4-dimethyl-5-isoxazolyl)-1-naphthalenesulfonamide
- Irbesartan
- Bosentan
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Topics |
- Angiotensin II
(adverse effects)
- Animals
- Animals, Genetically Modified
- Antihypertensive Agents
(pharmacology)
- Biphenyl Compounds
(pharmacology)
- Bosentan
- Cardiomyopathies
(etiology, pathology, physiopathology)
- Dansyl Compounds
(pharmacology)
- Disease Models, Animal
- Endothelin-1
(drug effects, physiology)
- Fibrosis
(etiology, pathology, physiopathology)
- Hypertension
(chemically induced, complications, physiopathology)
- Irbesartan
- Male
- Rats
- Receptor, Angiotensin, Type 1
- Receptors, Angiotensin
(drug effects, physiology)
- Receptors, Cell Surface
(drug effects, physiology)
- Sulfonamides
(pharmacology)
- Tetrazoles
(pharmacology)
- Time Factors
- Vasoconstrictor Agents
(adverse effects)
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