Document Detail


Angiotensin-(1-9) regulates cardiac hypertrophy in vivo and in vitro.
MedLine Citation:
PMID:  20411619     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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
Related Documents :
22088859 - Novel method to evaluate the conduction velocity and conducting area during isthmus-dep...
1529929 - Role of nitrates in acute myocardial infarction.
12716649 - An easy and safe way of left ventriculotomy closure in patients with left ventricle thr...
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of hypertension     Volume:  28     ISSN:  1473-5598     ISO Abbreviation:  J. Hypertens.     Publication Date:  2010 May 
Date Detail:
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    
Other Details:
Languages:  eng     Pagination:  1054-64     Citation Subset:  IM    
Affiliation:
Departamento de Enfermedades Cardiovasculares, Escuela de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile. mocaran@med.puc.cl
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Angiotensin I / blood,  pharmacology*,  physiology
Angiotensin II / analogs & derivatives,  pharmacology
Angiotensin II Type 1 Receptor Blockers / pharmacology
Angiotensin-Converting Enzyme Inhibitors / pharmacology
Animals
Benzimidazoles / pharmacology
Bradykinin / blood
Cardiomegaly / etiology*,  pathology,  physiopathology,  prevention & control
Cell Enlargement / drug effects
Cells, Cultured
Enalapril / pharmacology
Humans
Hypertrophy, Left Ventricular / pathology,  physiopathology,  prevention & control
Insulin-Like Growth Factor I / pharmacology
Male
Myocardial Infarction / drug therapy,  pathology,  physiopathology
Myocytes, Cardiac / drug effects,  pathology
Norepinephrine / pharmacology
Peptide Fragments / blood,  pharmacology*,  physiology
Peptidyl-Dipeptidase A / metabolism
Rats
Rats, Sprague-Dawley
Renin-Angiotensin System / drug effects,  physiology
Tetrazoles / pharmacology
Ventricular Function, Left / drug effects
Chemical
Reg. No./Substance:
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 3.4.15.1/Peptidyl-Dipeptidase A; S8Q36MD2XX/candesartan

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Cardiovascular protective effects of nebivolol in Zucker diabetic fatty rats.
Next Document:  Severe obstructive sleep apnea elicits concentric left ventricular geometry.