Cardiac pro-inflammatory cytokines, NO system and oxidative stress in a fetal programming model of hypertension induced by moderate zinc deficiency since fetal life.

ARRANZ CRISTINA; JURIOL LORENA; GOBETTO NATALIA; PINEDA GONZALO; MENDES GARRIDO FACUNDO; WENK G; CARRANZA MA; ELESGARAY ROSANA; TOBLLI J; TOMAT ANALÍA

Congreso; 25th European Meeting on Hypertension and Cardiovascular Protection.; 2015

Moderate zinc deficiency during intrauterine and postnatal growth is a fetal programming model of hypertension, renal and cardiovascular dysfunction. Male zinc deficient rats showed reduced left ventricular (LV) wall thickness and ejection fraction. The aim of this study was to evaluate, nitric oxide (NO) system, pro­inflammatory cytokines and oxidative state in LV of adult male rats exposed to this deficiency. Wistar rats received during pregnancy up to weaning low (L:8 ppm) or control (C:30 ppm) zinc diet. After weaning, male offspring fed low (l) or control (c) zinc diet during 60 days (Cc, Ll, Lc). At day 81, we evaluated in LV: Interleukin­6 and Tumor Necrosis Factor­α (IL­6, TNF­α), basal NO synthase (NOS) and endothelial (eNOS), neuronal (nNOS) and inducible (iNOS) isoforms activities; eNOS and Ser1177 eNOS phosphorylation protein expression (eNOS/β­actin, pSer1177eNOS/eNOS), mRNA expression (eNOS/GAPDH) and lipid peroxidation end products levels (TBARS). Values are means±SEM, n=6/group. One way ANOVA, Bonferroni post­test.*p