Progressive cardiovascular autonomic dysfunction in rats with evolving metabolic syndrome

Metabolic syndrome is linked to increased cardiovascular mortality, which may be partially attributed to cardiac sympatho-vagal imbalance. However, autonomic changes were not evaluated during the metabolic syndrome development in a monosodium glutamate-induced animal model. We evaluate temporal changes in cardiovascular autonomic modulation in an animal model of metabolic syndrome. Eighteen neonate male spontaneously hypertensive rats (SHR) were treated with monosodium glutamate (MetS), and compared with Wistar–Kyoto (C) and saline-treated SHR (H). Lee index, insulin resistance and autonomic control (spectral analysis) were evaluated at 3 (3-mo), 6 (6-mo) and 9 (9-mo) months of age (compared by two-way ANOVA, p < 0.05). Weight of visceral fat, Lee index and arterial pressure were higher in the MetS vs. C and H groups (p < 0.001) at all ages. Heart rate variability (HRV) was decreased in the MetS and H groups at 3-mo and 9-mo vs. C. The LF component of HRV was reduced in the MetS group at 3-mo vs. C (p = 0.032), and higher vs. C and H at 9-mo (p < 0.001, all comparisons). H and MetS rats had a higher LF/HF index vs. C at 9-mo (p = 0.001, all comparisons). The VLF component of systolic arterial pressure variability of the MetS was higher earlier (6-mo) than that of the H group. A reduction of 70%, 98% and 54% in αLF index of H and MetS rats vs. C, was observed at 3, 6 and 9 months, respectively. Metabolic syndrome and hypertension in rats evolve with progressive autonomic dysfunction (worst at 9 months), with specific derangements occurring very early.