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Myocardial hypertrophy induced by high salt consumption is prevented by angiotensin II type 2 receptor agonist

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Author(s):
Ellen Priscila Brito Dopona
Total Authors: 1
Document type: Doctoral Thesis
Press: São Paulo.
Institution: Universidade de São Paulo (USP). Faculdade de Medicina (FM/SBD)
Defense date:
Examining board members:
Joel Claudio Heimann; Maria Luiza Morais Barreto de Chaves; Rildo Aparecido Volpini
Advisor: Joel Claudio Heimann
Abstract

High salt intake is one of the main risk factors for the development of cardiovascular diseases. Dietary salt overload was found to increase cardiac angiotensin II content. Many studies have evaluated the role of angiotensin II on the development of cardiac hypertrophy and fibrosis. Angiotensin II acts through two main receptors: angiotensin II type 1 (AT1) and type 2 (AT2) receptors. Though there are many studies pointing to the effects of the AT1 and high salt diet, the role of AT2 and its effects in dietary salt overload model is still not elucidated. Aiming to better understand the role of AT2 receptor in models of salt overload on cardiac hypertrophy and fibrosis, male Wistar rats were fed normal or high salt diet from weaning up to 18 weeks of age. Both groups were divided into two subgroups. Starting at 7 weeks of age they were treated or not with compound 21 (3mg/kg per day, n=16), an AT2 receptor agonist. Body weight, blood pressure, food intake, water intake, urine volume, plasma and urinary sodium and potassium, cardiomyocyte transverse diameter, percentage of cardiac fibrosis, gene and protein expression of renin, angiotensinogen, angiotensin converting enzyme, AT1 and AT2 were measured. Compound 21 prevented the development of cardiac hypertrophy and fibrosis in rats that received high salt diet. Compound 21 also reduced the increased blood pressure, prevented the lower weight gain in animals fed with high salt diet (AU)

FAPESP's process: 13/08418-4 - Evaluation of intracellular cardiac renin-angiotensin system induced by high salt consumption
Grantee:Ellen Priscila Brito Dopona
Support Opportunities: Scholarships in Brazil - Doctorate (Direct)