Abstract P524: Vasoprotective Effect of Hesperidin in the Onset of Arterial Hypertension Induced by L-NAME

• DOI: 10.1161/hyp.70.suppl_1.p524
• Publication Date: 2021-07-03T08:06:48Z
• Authors: Fernanda Priviero; Tiago Tomazini Go...; Carolina Martins ...; Jackeline Mezencio; Natiele Araujo; Mario A Claudino; Patricia Carvalho; R Clinton Webb
• Keywords: 03 medical and health sciences; 0302 clinical medicine; 3. Good health

Hesperidin has been used to manage venous disease and has been shown to have vasodilator, antiinflammatory and antioxidant properties. The aim of this work was to evaluate the efects of acute treatment with hesperidin (HD) on the vascular reactivity of rats in the onset of arterial hypertension induced by L-NAME. Male Wistar rats were divided into 3 groups as follow: 1- Control (CTL); 2- L-NAME (LN); 3- L-NAME + Hesperidin (LNHD). LN was given by gavage at the dose of 75mg/Kg, concomitantly with HD at the dose of 0.5 mmol/Kg, 24 hours previously to the sacrifice. After sacrifice, the blood was collected and the aorta removed and mounted in a wire myograph to assess concentration response curves to acetylcholine (ACh) and sodium nitroprusside (SNP). ACh elicited concentration dependent relaxation in aorta of CTL rats, reaching a maximum relaxation of 89 ± 3%, which was significantly reduced in LN group (37 ± 7%). Treatment with HD partially prevented this decrease, reaching the maximum relaxation of 72 ± 2%. On the other hand, SNP induced relaxation was more potent on the aorta of LN (pEC 50 9.67 ± 0.11) when compared to CTL (pEC 50 8.51 ± 0.13) and LNHD rats (pEC 50 8.90 ± 0.09). The oxidative status was not changed by any treatment since SOD activity was 11 ± 1, 9 ± 2 and 12 ± 0.5 U/mL, for CTL, LN and LNHD, respectively and lipid peroxidation measured by TBARS assay showed a MDA concentration of 29 ± 8, 35 ± 7 and 23 ± 3 μM for CTL, LN and LNHD, respectively. Altogether, these data suggest that that Hesperidin prevents the impairment of endothelium-dependent vascular relaxation, through a mechanism not related to its antioxidant property.