Tungstate and vanadium effects on blood pressure in fructose-overloaded rats

PEREDO, HORACIO A; CARRANZA, ANDREA; MAYER, MARCOS A; ZABALZA, MARÍA; PUYÓ, ANA MARÍA

Milan, Italy

Congreso; 19th European Meeting on Hypertension; 2009

<!-- /* Style Definitions */ p.MsoNormal, li.MsoNormal, div.MsoNormal {mso-style-parent:""; margin:0in; margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:12.0pt; font-family:"Times New Roman"; mso-fareast-font-family:"Times New Roman";} @page Section1 {size:8.5in 11.0in; margin:1.0in 1.25in 1.0in 1.25in; mso-header-margin:.5in; mso-footer-margin:.5in; mso-paper-source:0;} div.Section1 {page:Section1;} --> Tungstate and vanadium effects on blood pressure in fructose overloaded-rats   Carranza A, Peredo HA, Mayer MA, Zabalza M, Puyo AM   Sodium tungstate (T) and vanadyl sulfate (V) show insulinomimetic effects in diabetic rats. Fructose overload induces in the rat insulin resistance, hypertension and dyslipidemia, resembling the human metabolic syndrome. In previous studies we found alterations in vascular production of vasoactive prostanoids in this model. Our objective was to analyze the effect of the treatments with T and V on blood pressure, metabolic parameters and prostanoid release in mesenteric vascular bed from fructose-overloaded rats. Male Sprague-Dawley rats were divided in 6 groups; Control (C, tap water, n=6) < Fructose (F, 10% w/v F solution in the drinking water, n=6); C-T (T solution, 2g/l, n=7); F-T (both treatments, n=6); C-V (V solution, 100 mg/ml), n=6) and F-V (both treatments, n=7). All treatments were administrated for 9 weeks. Systolic blood pressure was measure by the tail-cuff method, glycemia and plasma TG by enzymatic assay and vascular release of prostanoids by HPLC. Fructose increased blood pressure (mmHg, F: 128±2 vs. C: 116±2, p<0.01), glycemia (mg/dl, F: 148±5 vs. C: 123±6, p<0.01) and triglyceridemia (mg/dl, F: 191±35 vs. C: 94±23, p<0.05). Fructose reduced the vasodilator prostacyclin (PGI2, ng/mg tissue, F: 56±12 vs. C: 100±8, p<0.05) and prostaglandin (PG)E2 (F: 38±8 vs. C: 92±8, p<0.005). T prevents the increase in blood pressure (F-T: 115±2 vs. F, p<0.001), glycemia (FT: 126±4, p<0.001) and triglyceridemia (F-T: 100±10 vs. F, p<0.05) and also the decrease in prostanoid production: PGI2 (F-T: 106±11 vs. F, p<0.005); PGE2 (F-T: 102±9 vs. F, p<0.005). V treatment increased blood pressure in C (C-V: 136±4 vs. C, p<0.01) with no effects on F(F-V: 143±7) and did not prevent metabolic alterations. T did not modify and parameter in C. Body weight and plasma HDL cholesterol remained unchanged in all groups. T treatment prevents hypertension, metabolic alterations and the imbalance in the vascular production of vasoactive prostanoids caused by fructose overload in the rat, meanwhile V not only is ineffective but also increases blood pressure in control animals.