Effects of prenatal and postnatal zinc deficiency on the vascular function of adult male and female rats.

MENDES GARRIDO FACUNDO; GOBETTO NATALIA; JURIOL LORENA; ELESGARAY ROSANA; TOMAT ANALÍA; ARRANZ CRISTINA

Congreso; IMBS II International Congress of Translational Medicine. Cellular and molecular pathways as therapeutic targets; 2015

In previous studies, we demonstrated that moderate zinc deficiency during fetal and postnatal life induces low birth weight and programs cardiovascular and renal disorders in adult life, associated with increased systolic blood pressure in male rats and decreased activity of endothelial nitric oxide (NO) synthase in vascular tissue of both sexes.Objective:We evaluated vascular function in adult male and female rats exposed to fetal and postnatal zinc deficiency. Methods:Female Wistar rats received during pregnancy up to weaning low (L: 8ppm) or control (C: 30ppm) zinc diet. After weaning, male (m) and female (f) L offspring fed low (l) or control (c) zinc diet during 60 days (Llm, Llf, Lcm, Lcf). C offspring fed control (c) zinc diet (Ccm, Ccf) during 60 days. At day 81, animals were sacrificed and the thoracic aorta was removed. Aortic rings were suspended in Krebs solution at 37°C bubbled with carbogen gas to evaluate the constriction with phenylephrine (PE, 10-9 to 10-5M) or angiotensin II (AngII, 10-10 to 10-6M). To evaluate endothelium-independent relaxation, ACh protocol was also performed in endothelium-denuded rings. The maximal response (Rmax) to PE and AngII was expressed as % of maximum contraction achieved with 90mM KCl. We analyzed relaxation with acetylcholine (ACh,10-10 to 10-3M) or sodium nitroprusside (SNP, NO donor,10-13 to 10-5M) in rings preconstricted with PE 10-5M. The maximal relaxation to ACh and SNP was expressed as % of PE constriction. NADPH oxidase activity was measured using a chemiluminescence method. Statistics: Two way ANOVA, Bonferroni post-test, data as mean±SEM, *p