OBJECTIVES: The aim of this study was to evaluate cardiovascular autonomic function in a rodent obesity model induced by monosodium glutamate injections during the first seven days of life. METHOD: The animals were assigned to control (control, n = 10) and monosodium glutamate (monosodium glutamate, n = 13) groups. Thirty-three weeks after birth, arterial and venous catheters were implanted for arterial pressure measurements, drug administration, and blood sampling. Baroreflex sensitivity was evaluated according to the tachycardic and bradycardic responses induced by sodium nitroprusside and phenylephrine infusion, respectively. Sympathetic and vagal effects were determined by administering methylatropine and propranolol. RESULTS: Body weight, Lee index, and epididymal white adipose tissue values were higher in the monosodium glutamate group in comparison to the control group. The monosodium glutamate-treated rats displayed insulin resistance, as shown by a reduced glucose/insulin index (-62.5%), an increased area under the curve of total insulin secretion during glucose overload (39.3%), and basal hyperinsulinemia. The mean arterial pressure values were higher in the monosodium glutamate rats, whereas heart rate variability (>7 times), bradycardic responses (>4 times), and vagal (~38%) and sympathetic effects (~36%) were reduced as compared to the control group. CONCLUSION: Our results suggest that obesity induced by neonatal monosodium glutamate treatment impairs cardiac autonomic function and most likely contributes to increased arterial pressure and insulin resistance.

OBJECTIVE: High fructose consumption contributes to the incidence of metabolic syndrome and, consequently, to cardiovascular outcomes. We investigated whether exercise training prevents high fructose diet-induced metabolic and cardiac morphofunctional alterations. METHODS: Wistar rats receiving fructose overload (F) in drinking water (100 g/l) were concomitantly trained on a treadmill (FT) for 10 weeks or kept sedentary. These rats were compared with a control group (C). Obesity was evaluated by the Lee index, and glycemia and insulin tolerance tests constituted the metabolic evaluation. Blood pressure was measured directly (Windaq, 2 kHz), and echocardiography was performed to determine left ventricular morphology and function. Statistical significance was determined by one-way ANOVA, with significance set at p<0.05. RESULTS: Fructose overload induced a metabolic syndrome state, as confirmed by insulin resistance (F: 3.6 ± 0.2 vs. C: 4.5 ± 0.2 mg/dl/min), hypertension (mean blood pressure, F: 118 ± 3 vs. C: 104 ± 4 mmHg) and obesity (F: 0.31±0.001 vs. C: 0.29 ± 0.001 g/mm). Interestingly, fructose overload rats also exhibited diastolic dysfunction. Exercise training performed during the period of high fructose intake eliminated all of these derangements. The improvements in metabolic parameters were correlated with the maintenance of diastolic function. CONCLUSION: The role of exercise training in the prevention of metabolic and hemodynamic parameter alterations is of great importance in decreasing the cardiac morbidity and mortality related to metabolic syndrome.

OBJETIVO: O objetivo do presente estudo foi investigar a modulação autonômica do sistema cardiovascular em ratos espontâneamente hipertensos (SHR) e diabéticos por estreptozotocina (STZ), avaliando a sensibilidade do reflexo barorreceptor e a variabilidade da pressão arterial e da freqüência cardíaca. MÉTODOS: Ratos SHR machos foram divididos em grupos controle (SHR) e diabéticos (SHR+DM, 5 dias após STZ). A pressão arterial (PA) e a sensibilidade dos barorreceptores (avaliada pelas respostas taquicárdicas e bradicárdicas a alterações da PA) foram monitoradas. Os sinais de pressão arterial sistólica (PAS) e o intervalo de pulso (IP) foram analisados no domínio do tempo e da freqüência pelo método autoregressivo sendo quantificados os componentes oscilatórios de baixa (BF: 0,2-0,6Hz) e alta (AF:0,6-3,0Hz) freqüência. RESULTADOS: A PA média e a freqüência cardíaca estavam reduzidas no grupo SHR+DM (131±3 mmHg e 276±6 bpm) em relação ao grupo SHR (160±7 mmHg e 330±8 bpm). A bradicardia reflexa a aumentos de PA estava atenuada no grupo SHR+DM quando comparada ao grupo SHR (0,55±0,1 vs 0,97±0,1 bpm/mmHg). A variabilidade da PAS no domínio do tempo (desvio padrão batimento-a-batimento da série temporal da PAS) foi menor no grupo SHR+DM (3,1±0,2 mmHg) quando comparada ao grupo SHR (5,7±0,6 mmHg). O desvio padrão do IP foi semelhante entre os grupos. O diabetes reduziu o componente BF da PAS (3,3±0,8 vs 28,7±7,6 mmHg² no SHR), mas não alterou o componente AF da PAS. Em relação aos componentes oscilatórios do IP não houve diferença entre os grupos. CONCLUSÕES: Estes resultados sugerem que a associação de hipertensão e diabetes causa uma importante diminuição da modulação simpática cardiovascular periférica que poderia, pelo menos em parte, ser responsável pela redução da PA. Além disso, este estudo demonstra que o diabetes pode, de fato, piorar a já reduzida função de tamponamento dos barorreceptores ao mesmo tempo em que reduz a pressão arterial.

OBJECTIVE: The aim of the present study was to evaluate the autonomic modulation of the cardiovascular system in streptozotocin (STZ)-induced diabetic spontaneously hypertensive rats (SHR), evaluating baroreflex sensitivity and arterial pressure and heart rate variability. METHODS: Male SHR were divided in control (SHR) and diabetic (SHR+DM, 5 days after STZ) groups. Arterial pressure (AP) and baroreflex sensitivity (evaluated by tachycardic and bradycardic responses to changes in AP) were monitored. Autoregressive spectral estimation was performed for systolic AP (SAP) and pulse interval (PI) with oscillatory components quantified as low (LF:0.2-0.6Hz) and high (HF:0.6-3.0Hz) frequency ranges. RESULTS: Mean AP and heart rate in SHR+DM (131±3 mmHg and 276±6 bpm) were lower than in SHR (160±7 mmHg and 330±8 bpm). Baroreflex bradycardia was lower in SHR+DM as compared to SHR (0.55±0.1 vs. 0.97±0.1 bpm/mmHg). Overall SAP variability in the time domain (standard deviation of beat-by-beat time series of SAP) was lower in SHR+DM (3.1±0.2 mmHg) than in SHR (5.7±0.6 mmHg). The standard deviation of the PI was similar between groups. Diabetes reduced the LF of SAP (3.3±0.8 vs. 28.7±7.6 mmHg2 in SHR), while HF of SAP were unchanged. The power of oscillatory components of PI did not differ between groups. CONCLUSIONS: These results show that the association of hypertension and diabetes causes an impairment of the peripheral cardiovascular sympathetic modulation that could be, at least in part, responsible for the reduction in AP levels. Moreover, this study demonstrates that diabetes might actually impair the reduced buffer function of the baroreceptors while reducing blood pressure.