Navegando por Palavras-chave "Renin angiotensin system"

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    Early developmental exposure to high fructose intake in rats with NaCl stimulation causes cardiac damage
    (Springer Heidelberg, 2016) Araujo, I. C. [UNIFESP]; Andrade, R. P.; Santos, F.; Soares, E. S.; Yokota, R. [UNIFESP]; Mostarda, C.; Fiorino, P.; De Angelis, K.; Irigoyen, M. C.; Morris, M.; Farah, V. [UNIFESP]
    Metabolic syndrome (MS) increases the risk of type 2 diabetes and cardiovascular disease. High consumption of fructose is a proposed cause of increased MS, manifested through hypertension, obesity, insulin resistance, and dyslipidemia. High NaCl also increases the risk of CD. The purpose of this study is to evaluate the influence of fructose and sodium on autonomic dysfunction and its relation with CD in MS. Fructose overload was started at weaning and continued through adulthood. Male Wistar rats (21 days) were divided into four groups: Control (C), fructose consumption (10 %, F), NaCl consumption (salt 1 % for the 10 last days, S), and fructose and NaCl (FS), and monitored for 8 weeks. Metabolic evaluations consisted of Lee index, glycemia, insulin and glucose tolerance tests, triglycerides, and total cholesterol measurements. Cardiovascular parameters measured were arterial pressure (AP) and cardiac function performed by echocardiography. They also measured the influence of renin angiotensin (RAS) and autonomic nervous systems by drug blockage with losartan, atropine, and atenolol. Energy analysis showed no change between groups. Fructose overload induced a MS state, confirmed by insulin resistance, glucose intolerance, and dyslipidemia. Fasting glucose was increased in F and FS rat groups compared with C and S groups. AP was higher in F, S, and FS groups in comparison with the C group. The hypotensive response after sympathetic blockade was increased in F, S, and FS versus C. The cardiac vagal tonus was reduced in F and FS animal groups. The intrinsic heart rate was decreased in the FS group (372 +/- A 9 bpm) compared with the C group (410 +/- A 13 bpm). The morphometric measurements evaluated through left ventricular diameter during diastole and the left ventricular diameter during systole decreased in the FS group (16 and 26 %, respectively). Diastolic function was reduced in F and FS. The depressor response induced by losartan was increased in the F group in comparison with other groups. However, there was a uniform increase in plasma ACE activity in all treated groups compared with the C group. Data suggest that early exposure to high fructose intake produced marked alterations in metabolic and cardiovascular function. When stimulated by NaCl, the fructose-fed subjects showed further impairment in cardiac function.
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    Early developmental exposure to high fructose intake in rats with NaCl stimulation causes cardiac damage
    (Springer Heidelberg, 2016) Araujo, I. C. [UNIFESP]; Andrade, R. P.; Santos, F.; Soares, E. S.; Yokota, R. [UNIFESP]; Mostarda, C.; Fiorino, P.; De Angelis, K.; Irigoyen, M. C.; Morris, M.; Farah, V. [UNIFESP]
    Metabolic syndrome (MS) increases the risk of type 2 diabetes and cardiovascular disease. High consumption of fructose is a proposed cause of increased MS, manifested through hypertension, obesity, insulin resistance, and dyslipidemia. High NaCl also increases the risk of CD. The purpose of this study is to evaluate the influence of fructose and sodium on autonomic dysfunction and its relation with CD in MS. Fructose overload was started at weaning and continued through adulthood. Male Wistar rats (21 days) were divided into four groups: Control (C), fructose consumption (10 %, F), NaCl consumption (salt 1 % for the 10 last days, S), and fructose and NaCl (FS), and monitored for 8 weeks. Metabolic evaluations consisted of Lee index, glycemia, insulin and glucose tolerance tests, triglycerides, and total cholesterol measurements. Cardiovascular parameters measured were arterial pressure (AP) and cardiac function performed by echocardiography. They also measured the influence of renin angiotensin (RAS) and autonomic nervous systems by drug blockage with losartan, atropine, and atenolol. Energy analysis showed no change between groups. Fructose overload induced a MS state, confirmed by insulin resistance, glucose intolerance, and dyslipidemia. Fasting glucose was increased in F and FS rat groups compared with C and S groups. AP was higher in F, S, and FS groups in comparison with the C group. The hypotensive response after sympathetic blockade was increased in F, S, and FS versus C. The cardiac vagal tonus was reduced in F and FS animal groups. The intrinsic heart rate was decreased in the FS group (372 +/- A 9 bpm) compared with the C group (410 +/- A 13 bpm). The morphometric measurements evaluated through left ventricular diameter during diastole and the left ventricular diameter during systole decreased in the FS group (16 and 26 %, respectively). Diastolic function was reduced in F and FS. The depressor response induced by losartan was increased in the F group in comparison with other groups. However, there was a uniform increase in plasma ACE activity in all treated groups compared with the C group. Data suggest that early exposure to high fructose intake produced marked alterations in metabolic and cardiovascular function. When stimulated by NaCl, the fructose-fed subjects showed further impairment in cardiac function.
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    Structural analysis of three peptides related to the transmambranic helix VI of AT1 receptor
    (Churchill Livingstone, 2010-04-01) Ribeiro de Noronha, Samuel Marcos [UNIFESP]; Corrêa, Silvana Aparecida Alves [UNIFESP]; Poletti, Erick Fernando; Lopes, Douglas Duarte; Silva, Caroline Correa da; Sforca, Mauricio Luis; Shimuta, Suma Imura; Tonin Zanchin, Nilson Ivo; Nakaie, Clovis Ryuichi; Cotrim Guerreiro da Silva, Ismael Dale; Universidade Federal de São Paulo (UNIFESP); Dept Biofis; Lab Nacl Luz Sincroton
    Introduction: Angiotensin II (AII) is the main active product of the renin angiotensin system. Better known effects of All are via AT1 receptor (AT1R). Expression of AT1R mutants (L265D and L262D) in CHO cells increased cAMP formation when compared to CHO cells expressing the wild type (WT) AT1R. Morphological transformation of CHO cells transfected with mutants correlated with their increased cAMP formation. DNA synthesis was inhibited in these cells too, indicating that cAMP promotes inhibitory effects on transfected CHO cells growth and causes their morphological change from a tumorigenic phenotype to a non-tumorigenic one.Objectives: To assess the importance of leucine 262 and 265 in determining AT1R structure by means of a comparative structural analysis of two mutant peptides and of a wild-type fragment.Methodology: Three peptides had their conformation compared by circular dichroism (CD): L262D(259-272). L265D(259-272) (mutants) and WT(260-277).Results: Secondary structures were: beta-turn for WT and L262D and random coil for L265D.Conclusions: Strong correlation was found in the results of biochemical, cellular and structural approaches used to compare WT AT1R to mutant types. Random coil structure of the L265D mutant may be a key point to explain those changes observed in biochemical (binding and signal transduction) and proliferation assays (Correa et al., 2005). beta-Turn formation is an important step during early protein folding and this secondary simple structure is present in L262D and WT, but not in L265D. Therefore, leucine 265 seems to play a crucial role in determining an entirely functional AT1R. (C) 2009 Elsevier B.V. All rights reserved.