Prenatal and postnatal zinc deficiency programs endotelial dysfunction in male rats. (Trabajo premiado)

MENDES-GARRIDO F; JURIOL L; GOBETTO MN; WENK G; BRUNELLO F; CANIFFI C; ELESGARAY R; TOMAT AL; ARRANZ C

Foz de Iguazú

Congreso; 1st PanAmerican Congress of Physiological Sciences; 2014

Physiology Societies

Moderate zinc deficiency during intrauterine and postnatal growth induces an increase in systolic blood pressure (SBP), cardiac and renal alterations. We evaluated aortic nitric oxide (NO) production and vascular function in adult male rats exposed to fetal and postnatal zinc deficiency. Female Wistar rats received during pregnancy up to weaning low(L:8ppm) or control(C:30ppm) zinc diet. After weaning, male offspring fed low (l) or control (c) zinc diet during 60 days (Cc,Ll,Lc). At day 81, we measured NO synthase (NOS) activity (pmol 14C-L-citrulline/g.tissue.min, 14C-L-Arginine method) in thoracic aorta. In aortic rings suspended in Krebs solution and preconstricted with phenylephrine (10-5M), we evaluated the relaxation with acetylcholine(ACh,10-10-10-3M) or sodium nitroprusside(SNP,NO donor,10-13-10-5M). To evaluate endothelium-independent relaxation, ACh protocol was also performed in endothelium-denuded rings. Statistics: One way ANOVA, Bonferroni post-test,*p<0.01 vs Cc (n=6/group). Ll and Lc rats showed a decrease in aortic NOS activity (Cc:225±5, Ll:172±4*, Lc:160±8*). In aortic rings, ACh maximal relaxation was 21% and 15% lower in Ll and Lc respectively, compared to Cc, and it was completely abolished in endothelium-denuded rings. No differences were observed in SNP relaxation. Zinc deficiency during fetal and postnatal life programs an impaired vasodilator capacity due to a lower endothelial NO production that could contribute to SBP elevation in adult life. Supported by:UBA-CONICET