Fetal programming of hypertension induced by zinc restriction in fetal life: Gender differences in early effects on kidney

ARRANZ C; AGUIRRE S; VEIRAS L; COSTA M.A; TOMAT, AL

Jackson, Mississippi

Congreso; APS Conference: Physiology of cardiovascular disease: Gender disparities; 2011

American Physiology Society

We have shown that moderate zinc deficiency during fetal and postnatal growth induced hypertension and renal diseases in adults.Aim: To evaluate renal oxide synthase (NOS) activity and oxidative stress at 21 days of life and sex differences in the response to fetal and lactation zinc deficiency.Methods: It was determined renal NOS activity with L-(U14C)-arginine (pmol/ming tissue) and protein abundance by western blot (% density/beta actin), renal thiobarbituric acid-reactive substances (TBARS), glutathione concentration (GLUT), superoxide dismutase (SOD), catalase (CAT) and glutathione reductase activity (GPx) in 21 days female (f) and male (m) offspring of Wistar rats exposed from pregnancy up to weaning: low(L,8 ppm) or control(C,30 ppm) zinc diet ( n=6).Results: Renal NOS activity was decreased in Bm (237±5) and Bf (245±7) compared with Cm (302±5) and Cf (317±11) respectively. It was not associated with lower expression of eNOS, nNOS, iNOS protein. *p<0.01vs Cm; ? p<0.01vs Cf.Kidney morphological alterations observed in this model may be associated with nitric oxide system and oxidative stress alterations The lower renal NOS activity is not due to a decrease in protein expression so we suggest that other mechanisms may be involved, like alteration in NOS zinc cluster, cofactors or the oxidative stress. The impairment of antioxidant enzymes due to this deficiency is more evident in female than in male rats