Moderate zinc deficiency during growth and the expression of cardiovascular risck factors in adult life.

ARRANZ CRISTINA; TOMAT ANALIA; ZAGO VALERIA; ELESGARAY ROSANA; GONZALEZ AGUSTÍN; PRENTKI SANTOS ESTEFANIA; BALASZCZUK ANA MARÍA; COSTA MARIA DE LOS ANGELES

Milan Italia

Congreso; Seventeenth European Meeting on Hypertension.; 2007

European Society of Hypertension

Background: In previous studies we showed that moderate zinc deficiency during post-weaning growth in rats induced an increase in systolic blood pressure (SBP) associated with a decrease in the vascular and renal nitric oxide (NO) system and renal morphological and functional alterations in the adult life. Objective: We studied the effects of moderate zinc deficiency during fetal and early postnatal life on SBP, lipid metabolism, cardiovascular NO system activity and cardiac oxidative stress state in the adult life. Methods: Wistar rats received from the beginning of pregnancy up to weaning low (8 ppm) or control (30 ppm) zinc diet. After weaning, male offspring of each group of mothers continued with low (Cl and Ll) or control (Cc and Lc) zinc diet during 60 days. We determined: birth weight, SBP, plasmatic triglycerides (TG), total cholesterol (CHO), NADPH diaphorase (NADPH-d) activity (NO synthase activity marker) in heart and aorta, gluthation (GLUT) concentration, superoxide dismutase enzyme (SOD) activity and gluthation peroxidase (GPx) activity in cardiac tissue. Conclusions: Zinc deficiency during gestational period results in low birth weight offspring, which is associated with higher values of SBP in adult life. The increase in plasmatic TG induced by post-weaning zinc deficiency does not depend on zinc intake during fetal life. Zinc deficiency during fetal and/or postnatal growth induced a decrease in cardiovascular NO bioavailability, probably due to a lower activity of NO synthase and/or increase in cardiac reactive oxygen species. However, and adequate zinc intake during growth could neither totally revert the reduction of NO system activity nor reduce cardiac oxidative stress levels. Our results show that inadequate zinc intake during fetal life, lactation and growth could induce the expression of hypertension risk factors in the adult life.