|Angiotensin-(1-9) regulates cardiac hypertrophy in vivo and in vitro.|
|PMID: 20411619 Owner: NLM Status: MEDLINE|
|BACKGROUND: Angiotensin-(1-9) is present in human and rat plasma and its circulating levels increased early after myocardial infarction or in animals treated with angiotensin-converting enzyme inhibitor. However, the cardiovascular effects of this peptide are unknown.
OBJECTIVE: To determine whether angiotensin-(1-9) is a novel anti-cardiac hypertrophy factor in vitro and in vivo and whether this peptide is involved in the pharmacological effects of cardiovascular drugs acting on the renin-angiotensin system.
METHODS AND RESULTS: The administration of angiotensin-(1-9) to myocardial infarcted rats by osmotic minipumps (450 ng/kg per min, n = 6) vs. vehicle (n = 8) for 2 weeks decreased plasma angiotensin II levels, inhibited angiotensin-converting enzyme activity and also prevented cardiac myocyte hypertrophy. However, cardiac myocyte hypertrophy attenuation triggered by angiotensin-(1-9) was not modified with the simultaneous administration of the angiotensin-(1-7) receptor antagonist A779 (100 ng/kg per min, n = 6). In experiments in vitro with cultured cardiac myocytes incubated with norepinephrine (10 micromol/l) or with insulin-like growth factor-1 (10 nmol/l), angiotensin-(1-9) also prevented hypertrophy. In other experimental setting, myocardial infarcted rats (n = 37) were randomized to receive either vehicle (n = 12), enalapril (10 mg/kg per day, n = 12) or angiotensin II receptor blocker candesartan (10 mg/kg per day, n = 13) for 8 weeks. Both drugs prevented left ventricle hypertrophy and increased plasma angiotensin-(1-9) levels by several folds. Angiotensin-(1-9) levels correlated negatively with different left ventricular hypertrophy markers even after adjustment for blood pressure reduction.
CONCLUSION: Angiotensin-(1-9) is an effective and a novel anti-cardiac hypertrophy agent not acting via the Mas receptor.
|Maria Paz Ocaranza; Sergio Lavandero; Jorge E Jalil; Jaqueline Moya; Melissa Pinto; Ulises Novoa; Felipe Apablaza; Leticia Gonzalez; Carol Hernandez; Manuel Varas; Rene Lopez; Ivan Godoy; Hugo Verdejo; Mario Chiong|
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|Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't|
|Title: Journal of hypertension Volume: 28 ISSN: 1473-5598 ISO Abbreviation: J. Hypertens. Publication Date: 2010 May|
|Created Date: 2010-04-21 Completed Date: 2010-07-29 Revised Date: 2013-05-28|
Medline Journal Info:
|Nlm Unique ID: 8306882 Medline TA: J Hypertens Country: England|
|Languages: eng Pagination: 1054-64 Citation Subset: IM|
|Departamento de Enfermedades Cardiovasculares, Escuela de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile. email@example.com|
|APA/MLA Format Download EndNote Download BibTex|
Angiotensin II / analogs & derivatives, pharmacology
Angiotensin II Type 1 Receptor Blockers / pharmacology
Angiotensin-Converting Enzyme Inhibitors / pharmacology
Benzimidazoles / pharmacology
Bradykinin / blood
Cardiomegaly / etiology*, pathology, physiopathology, prevention & control
Cell Enlargement / drug effects
Enalapril / pharmacology
Hypertrophy, Left Ventricular / pathology, physiopathology, prevention & control
Insulin-Like Growth Factor I / pharmacology
Myocardial Infarction / drug therapy, pathology, physiopathology
Myocytes, Cardiac / drug effects, pathology
Norepinephrine / pharmacology
Peptide Fragments / blood, pharmacology*, physiology
Peptidyl-Dipeptidase A / metabolism
Renin-Angiotensin System / drug effects, physiology
Tetrazoles / pharmacology
Ventricular Function, Left / drug effects
|0/7-Ala-angiotensin (1-7); 0/Angiotensin II Type 1 Receptor Blockers; 0/Angiotensin-Converting Enzyme Inhibitors; 0/Benzimidazoles; 0/Peptide Fragments; 0/Tetrazoles; 0/angiotensin I (1-9); 11128-99-7/Angiotensin II; 51-41-2/Norepinephrine; 58-82-2/Bradykinin; 67763-96-6/Insulin-Like Growth Factor I; 75847-73-3/Enalapril; 9041-90-1/Angiotensin I; EC 126.96.36.199/Peptidyl-Dipeptidase A; S8Q36MD2XX/candesartan|
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