Dual ARB/NEP inhibition improved endothelial function in metabolic syndrome

D GARCIA, RODRIGO; M RAMIREZ MD, JESICA; PERAL DE BRUNO, MARIA; M MIATELLO, ROBERTO; F RENNA, NICOLAS

Trends in Research

OAT

Lugar: New York; Año: 2019 vol. 2 p. 1 - 6

DUAL ARB/NEP INHIBITION IMPROVED ENDOTHELIAL FUNCTION IN METABOLIC SYNDROME AbstractTo demonstrate that LZC696 (L) reduces organ damage in an experimental model of metabolic syndrome, were explored two mechanisms: anti-inflammatory effectsthrough the IL-6Ralpha pathway and through MAS1R, the production of endothelial repair mediated by VEGFR2+/CD133+ endothelial progenitor cells (EPCs).Experimental model of metabolic syndrome was realized by WKY rats and SHRs. SHR and WKY received a fructose diet in drinking water at 10% v/v for 12 weeks(FFHR and FFR receptivity). Chronic treatment with L: (68 mg / kg per day for 6 weeks) and valsartan (V) (34 mg / kg per day for 6 weeks, as control equimolargroup. Was determined: SBP, fast glycaemia and TTGO, left ventricular hypertrophy (HVI), vascular remodelling, hsCPR expression, and vascular expression inmesenteric tissue of IL-6Ralfa, STAT3, VEGFR2 and CD133 were determined. The experimental model was confirmed. L treatment reverted SBP, HVI, remodellingand vascular inflammation, decreased STAT3 expression and hsCPR in FFHR. Additionally, the most important finding was that L produced an increase in theexpression of resident EPCs in the endothelial tissue of mesenteric tissue.