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Moderate zinc deficiency during intrauterine and postnatal growth induces an increase in blood pressure levels, vascular remodelling and a decrease in vascular nitric oxide production in adult males.


The objective was to evaluate serum metabolic profile and aortic function in adult male rats exposed to fetal and postnatal zinc deficiency.

Design and method:

Female 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 (Cc, Ll, Lc).until 81 days of life.

Design and method:

At day 81, we measured systolic blood pressure (SBP,mmHg, tail-cuff technique), serum fasting glucose and lipid profile. In aortic rings suspended in Krebs solution we evaluated: maximal contraction (Rmax) to phenylephrine (PE, 10-9-10-5 M), angiotensin-II (Ang-II, 10-10-10-6 M) and caffeine (25 mM), expressed as % of maximal contraction with KCl 90 mM. In aortic rings preconstricted with PE 10-5 M, we measured the maximal relaxation with acetylcholine (ACh, 10-10-10-3 M) and sodium nitroprusside (SNP, nitric oxide donor, 10-11-10-5 M).


Values are means ± SEM, n = 6/group. One way ANOVA, Bonferroni post-test *p < 0.05 vs Cc; †p < 0.05 vs Lc.


Zinc deficiency during growth programs cardiovascular and metabolic risk factors in adult life. This nutritional injury during fetal and/or postnatal life programs a vascular hyporesponsiveness to ACh that could be due to the lower endothelial nitric oxide production as previously described. Moreover, a reduced contractile response to Ang-II and PE could be associated to alterations in intracellular calcium mobilization observed in caffeine experiments. Zinc deficiency during whole life would also induce metabolic disorders by increasing serum triglycerides and glucose levels. Adequate zinc content in the diet after weaning could prevent the metabolic but not all the vascular alterations induced by zinc restriction during fetal and early postnatal life.

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