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Autonomic dysfunction precede hemodynamic and metabolic changes in an experimental model of hypertension submitted to fructose overload
Author(s) -
Santos Camila Paixão,
Bernardes Nathalia,
Da Silva Dias Danielle,
Conti Filipe Fernandes,
Santos Fernando,
De Angelis Kátia
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.862.3
Subject(s) - medicine , hemodynamics , blood pressure , fructose , heart rate , endocrinology , mean arterial pressure , cardiology , diastole , pulse pressure , metabolic syndrome , heart rate variability , chemistry , obesity , biochemistry
The aim this study was to evaluate the effects of 7 days of fructose overload on metabolic, hemodynamic and autonomic parameters in spontaneous hypertensive rats. Male Wistar rats and SHR rats were divided into control (C), hypertensive (H) and hypertensive submitted to fructose overload (HF). The fructose overload (100g/L in drinking water) was started with 30 days of life of the animals. Arterial pressure (AP) signals were directly recorded. Cardiovascular autonomic modulation was evaluated by spectral analysis. Regarding metabolic evaluations, the glucose, insulin resistance and triglycerides were similar between studied groups. The mean arterial pressure, systolic AP and diastolic arterial pressure were higher in hypertensive animals (mean AP, H: 124±2 and HF: 123±3 mmHg) compared to the C group (mean AP: 95±2 mmHg). There was no difference in heart rate among groups. However, the HF group showed lower vagal modulation than C group, evidenced by a reduction in variance of pulse interval (HF: 12±2 vs. C: 37±8 ms 2 ) and RMSSD index (HF: 5.9±0.7 vs. C: 3.3±0.3 ms). Additionally, the HF group showed increase in variance of systolic arterial pressure compared to the C and H group (28 ± 4 vs. C: 13 ± 1 and H: 18 ± 2 mmHg 2 ). In conclusion, only 7 days of fructose overload was able to induce impairment in cardiac vagal modulation and vascular sympathetic modulation with no alteration on metabolic or hemodynamic parameters, suggesting that autonomic modulation dysfunction precede cardiometabolic changes in this experimental model of metabolic syndrome. Support or Funding Information FAPESP ‐ 2015/11223‐6; CAPES‐PROSUP – 1277269; UNINOVE, CNPq.

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