Abstract 614: Mechanism Involved In Fructose Induced Cardiovascular Risk: Evidence In An Experimental Model Of Hypertension And Menopause

Abstract

The metabolic syndrome is a bunch of ordinary pathologies: abdominal obesity associated to an excess of visceral fat, insulin resistance, dyslipidemia and hypertension. Moreover, the prevalence of hypertension and metabolic dysfunctions sharply increases after the menopause. However, the mechanisms involved in these changes were not well understood. Thus, the aim of this study was to evaluate the effects of ovarian hormone deprivation (9 wks) in hypertensive (or not) female rats submitted (or not) to fructose overload on cardiovascular autonomic control and cardiac oxidative stress. Female Wistar and SHR rats were divided into (n=8/group): control (C), ovariectomized (O), hypertensive ovariectomized (HO) and hypertensive ovariectomized submitted to fructose overload (100g/L in drinking water) (FHO). The arterial pressure (AP) signals were directly recorded. The cardiovascular autonomic modulation was evaluated by pharmacological blockade and by spectral analysis. Oxidative stress profile was evaluated by chemiluminescence (CL) and redox balance of glutathione (GSH/GSSG) determinations. The AP showed increased in the O and HO groups when compared to C group. The FHO group showed increased blood glucose and tryglicerides, insulin resistance; an additional increase in mean AP (174±4 vs. C:108±1; O:121±2; HO:164±5 mmHg), resting tachycardia, reduced vagal tonus (5±3 vs. C:55±5; O:37±6; HO:35±7bpm), increased sympathetic tonus (91±18 vs. 39±10bpm in C), decreased high frequency band of the pulse interval (vagal modulation) and exacerbated increased systolic AP variance and decreased low frequency band of the pulse interval (sympathetic modulation) in relation to other groups. The CL was higher in O and HO groups than C group. FHO group showed additional increase in CL (15043±1333 vs. C: 2661±358; O: 5134±277; HO: 6514±547 cps/mgprot) when compared to other groups. The cardiac GSH/GSSG was lower in FOH group (8.94±0.80 umol/g) in relation to HO group (13.0±1.4 umol/g), indicating impaired redox balance. In conclusion, the fructose overload induced metabolic dysfunctions associated with additional impairment in cardiovascular autonomic control and oxidative stress profile in hypertensive rats submitted to ovarian hormones deprivation.