Study of the renal rennin-angiotensin system in a fetal programming model of moderate zinc deficiency in male rats

GOBETTO MN; JURIOL L; MENDES-GARRIDO F; DASSO M; CARDELLI ALCALDE D; RADIONOVAS V; TOMAT AL; GIRONACCI M; ARRANZ C

Foz de Iguazú

Congreso; 1st PanAmerican Congress of Physiological Sciences; 2014

1st PanAmerican Congress of Physiological Sciences

We have previously demonstrated that a zinc deficient diet during pregnancy and/or growth induce hypertension and renal dysfunction in male rats. The aim of this study was to evaluate the renal renin-angiotensin system (RAS) in male rats exposed to a moderately zinc-deficient diet during fetal and/or postnatal growth. Wistar rats were exposed from early pregnancy until weaning of offspring to a zinc-deficient (L, 8ppm) or control (C, 30ppm) diet. At weaning, offspring continued with L or C diet for 60 days (CC,LC,LL). At day 81, we evaluated in renal tissue: AngII receptor (AT1R) by immunohistochemistry (IHC, positive staining/area of tissue %) and western blot (WB, optical density eNOS/â-actin relative to CC), angiotensin-converting enzyme (ACE) mRNA expression by RT-qPCR (ACE/GAPDH relative to CC), quantification of AngII by radioimmunoassay (RIA, pg/mg of tissue). Values are expressed as mean±SEM, n=6, one way ANOVA and Bonferroni post-hoc test. *p<0.05vsCC. Zinc deficiency induced an enhance of AT1 expression in cortex by IHC (CC: 7,9±1,7; LC: 13,3±2,9*; LL: 14,4±2,8*) and AT1 protein content (CC:1±0,2; LC:2,5±0,9*; LL:2,2±0,4*), an increase of Ang II (CC:1,0±0,13; LL:3,4±0,7*) and an increase in  renal ACE expression in LL (fold change: 6.4±0.6, p<0.001vsCC). Zinc restriction during fetal and early life induced an activation of the expression of renal RAS in male rats which may explain the development of hypertension and renal alterations observed previously.