Vascular risk factors programmed by zinc deficiency during prenatal and postnatal life in male rats

CASTAÑÓN, AGUSTINA; ARRANZ, CRISTINA; GOBETTO, NATALIA; TOMAT, ANALÍA; MENDES GARRIDO, FACUNDO; ELESGARAY, ROSANA

CABA

Congreso; XXIII Congreso Argentino de Hipertensión; 2016

Sociedad Argentina de Hipertensión Arterial

Background: Nutrient restriction during fetal growth may predispose to the development of hypertension in adult life. In Argentina 52% of pregnant women present an inadequate zinc intake (1). Our group has demonstrated that moderate zinc deficiency during intrauterine life and postnatal growth programs cardiac and renal alterations in adult life (2).Objective: We evaluated if zinc deficiency induces early vascular alterations in newborn rats that persist into adulthood.Methods: Wistar rats received during pregnancy up to weaning low (L:8ppm) or control (C:30ppm) zinc diet. At day 6 of life some L or C male offspring were sacrificed. After weaning, males fed low (l) or control (c) zinc diet (Cc, Ll, Lc) until day 81. We evaluated morphology of thoracic aorta and intrarenal resistance arteries (M/L, media/lumen areas ratio, Sirius red staining), activities of aortic Nitric Oxide Synthase (NOS, pmol 14C-L-Citrulline/g tissue.min) and NADPH oxidase (AU/g tissue, chemiluminescence method) and aortic lipid peroxidation (nmol MDA/mg prot, TBARS assay). At day 81 we measured systolic blood pressure (SBP,mmHg, tail-cuff technique). In aortic rings suspended in Krebs solution we evaluated maximal contraction to phenylephrine (PE,10-9-10-5M), angiotensin-II (Ang-II,10-10-10-6M) and caffeine (25mM) as % of KCl 90mM contraction. In rings preconstricted with PE 10-5M we measured the maximal relaxation with acetylcholine (ACh,10-10-10-3M) and sodium nitroprusside (SNP,NO donor,10-11-10-5M). Results: 6 daysLCBody weight (g)12.6±0.610.2±0.3*Renal arteries M/L4.1±0.46.8±0.5*Aortic M/L67±860±8NOS136±386±3*TBARS0.27±0.030.59±0.07* Student?s t-test,*p