JOEL CLAUDIO HEIMANN
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Clínica Médica, Faculdade de Medicina - Docente
LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina - Líder
LIM/16 - Laboratório de Fisiopatologia Renal, Hospital das Clínicas, Faculdade de Medicina - Líder
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conferenceObject Effect of an angiotensin II type 2 receptor agonist on myocardial hypertrophy and fibrosis induced by high salt diet(2017) DOPONA, Ellen Priscila Brito; ROCHA, Veronica Favoni; OLIVEIRA, Ivone Braga de; FURUKAWA, Luzia Naoko Shinohara; HEIMANN, Joel Claudio- Myocardial hypertrophy induced by high salt consumption is prevented by angiotensin II AT2 receptor agonist(2019) DOPONA, E. P. B.; ROCHA, V. F.; FURUKAWA, L. N. S.; OLIVEIRA, I. B.; HEIMANN, J. C.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.
- High-Salt Intake Induces Cardiomyocyte Hypertrophy in Rats in Response to Local Angiotensin II Type 1 Receptor Activation(2014) KATAYAMA, Isis A.; PEREIRA, Rafael C.; DOPONA, Ellen P. B.; SHIMIZU, Maria H. M.; FURUKAWA, Luzia N. S.; OLIVEIRA, Ivone B.; HEIMANN, Joel C.Many studies have shown that risk factors that are independent of blood pressure (BP) can contribute to the development of cardiac hypertrophy (CH). Among these factors, high-salt (HS) intake was prominent. Although some studies have attempted to elucidate the role of salt in the development of this disease, the mechanisms by which salt acts are not yet fully understood. Thus, the aim of this study was to better understand the mechanisms of CH and interstitial fibrosis (IF) caused by HS intake. Male Wistar rats were divided into 5 groups according to diet [normal salt (NS; 1.27% NaCl) or HS (8% NaCl)] and treatment [losartan. (LOS) (HS+LOS group), hydralazine (HZ) (HS+HZ group), or N-acetylcysteine (NAC) (HS+NAC group)], which was given in the drinking water. Tail-cuff BP, transverse diameter of the cardiomyocyte, IF, angiotensin II type 1 receptor (AT1) gene and protein expression, serum aldosterone, cardiac angiotensin II, cardiac thiobarbituric acid-reactive substances, and binding of conformation-specific anti-AT1 and anti-angiotensin II type 2 receptor (AT2) antibodies in the 2 ventricles were measured. Based on the left ventricle transverse diameter data, the primary finding was the occurrence of significant BP-independent CH in the HS+HZ group (96% of the HS group) and a partial or total prevention of such hypertrophy via treatment with NAC or LOS (81% and 67% of the HS group, respectively). The significant total or partial prevention of IF using all 3 treatments (HS+HZ, 27%; HS+LOS, 27%; and HS+NAC, 58% of the HS group, respectively), and an increase in the AT1 gene and protein expression and activity in groups that developed CH, confirmed that CH occurred via the AT1 in this experimental model. Thus, this study unveiled some relevant previously unknown mechanisms of CH induced by chronic HS intake in Wistar rats. The link of oxidative stress with CH in our experimental model is very interesting and stimulates further evaluation for its full comprehension.
conferenceObject Compound 21 Prevents Salt Induced Myocardial Hypertrophy(2016) DOPONA, Ellen Priscila Brito; FAVONI, Veronica; OLIVEIRA, Ivone Braga de; HEIMANN, Joel ClaudioconferenceObject Mechanisms of myocardial alterations induced by chronic high-salt intake(2012) KATAYAMA, Isis Akemi; DOPONA, Ellen Priscila Brito; HEIMANN, Joel Claudio