Myocardial hypertrophy induced by high salt consumption is prevented by angiotensin II AT2 receptor agonist

Imagem de Miniatura
Arquivos
art_DOPONA_Myocardial_hypertrophy_induced_by_high_salt_consumption_is_2019.PDF (533.04 KB)
Citações na Scopus
11
Tipo de produção
article
Data de publicação
2019
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
ELSEVIER SCI LTD
Autores
ROCHA, V. F.
Citação
NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES, v.29, n.3, p.301-305, 2019
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background and aims: Although many studies have reported the effects of AT1 receptor on dietary salt overload, the role of AT2 receptor in this model is far from completely elucidated. The present study aimed to better understand the role of AT2 receptor in cardiac structure alterations in response to chronic high salt intake in rats. Methods and results: Male Wistar rats were fed a normal or high salt diet from weaning until 18 weeks of age. Both groups were subdivided into two groups. Starting at 7 weeks of age, rats were treated with or without compound 21 (0.3 mg/kg/day, n = 16), an AT2 receptor agonist. Metabolics and structural parameters were measured. BP, transverse cardiomyocyte and intersticial fibrose was higher in animals fed with high salt diet compared with normal salt fed animals. Conclusion: Compound 21 prevented the development of cardiac hypertrophy and fibrosis, reduced the increase in blood pressure and prevented the lower weight gain in animals fed a high salt diet.
Palavras-chave
Salt, Blood pressure, Myocardial hypertrophy, Myocardial fibrosis, Compound 21
URI
https://observatorio.fm.usp.br/handle/OPI/31107
Referências
  1. Ali Q, 2015, AM J PHYSIOL-RENAL, V308, pF1379, DOI 10.1152/ajprenal.00002.2015
  2. BAKER KM, 1992, ANNU REV PHYSIOL, V54, P227, DOI 10.1146/annurev.physiol.54.1.227
  3. Cappuccio FP, 2013, KIDNEY INT SUPPL, V3, P312, DOI 10.1038/kisup.2013.65
  4. Coelho MS, 2006, NUTR METAB CARDIOVAS, V16, P148, DOI 10.1016/j.numecd.2005.09.001
  5. Ferreira DN, 2010, J NUTR, V140, P1742, DOI 10.3945/jn.109.117473
  6. Flores-Munoz M, 2012, HYPERTENSION, V59, P300, DOI 10.1161/HYPERTENSIONAHA.111.177485
  7. Jehle AB, 2012, J CARDIOVASC PHARM, V59, P363, DOI 10.1097/FJC.0b013e3182444110
  8. Kaschina E, 2014, CURR HYPERTENS REP, V16, DOI 10.1007/s11906-014-0441-0
  9. Kaschina E, 2008, CIRCULATION, V118, P2523, DOI 10.1161/CIRCULATIONAHA.108.784868
  10. Katayama IA, 2014, J NUTR, V144, P1571, DOI 10.3945/jn.114.192054
  11. Koulis C, 2015, HYPERTENSION, V65, P1073, DOI 10.1161/HYPERTENSIONAHA.115.05204
  12. Lemarie CA, 2010, J RENIN-ANGIO-ALDO S, V11, P19, DOI 10.1177/1470320309347785
  13. Olivotto I, 2008, J AM COLL CARDIOL, V52, P559, DOI 10.1016/j.jacc.2008.04.047
  14. Savoia C, 2007, HYPERTENSION, V49, P341, DOI 10.1161/01.HYP.0000253968.95136.b8
  15. Smyth A, 2015, CURR HYPERTENS REP, V17, DOI 10.1007/s11906-015-0559-8
  16. Wan YQ, 2004, J MED CHEM, V47, P5995, DOI 10.1021/jm049715t

Coleções
Artigos e Materiais de Revistas Científicas - FM/MCM
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - LIM/16
Artigos e Materiais de Revistas Científicas - ODS/03