Fetal programming of hypertension induced by zinc restriction during fetal life: early effects on heart.

ARRANZ C; VEIRAS L; AGUIRRE S; SANCHEZ R; CARDELLI ALCALDE D; COSTA MA; TOMAT AL

Oslo, Noruega

Congreso; 20th European Meeting on Hypertension; 2010

European Society of Hypertension

Objectives: Previously, we have shown that inadequate zinc intake during fetal life, lactation and/or post-weaning growth programs hypertension and, in kidney, a reduced nitric oxide (NO) system activity, a reduction in glomerular filtration surface area, an increase in oxidative stress, and the activation of apoptotic and fibrotic processes in the adult rats. The aim was to evaluate cardiac alterations in early periods of life in zinc deficient rats and to compare the effects in males (m) and females (f). Methods: Wistar rats received from the beginning of pregnancy up to myocytes length (mm), diameter (mm) and length to diameter ratio, and weaning, low(L, 8 ppm) or control(C, 30 ppm) zinc diet. At day 6 of birth, m and f offspring of each group of mothers (Cm, Lm, Cf and Lf) were sacrificed to determine heart weight (g/100 g body weight), cardiac NO synthase (NOS) activity with L-(U14C)-arginine (pmol Cit/g tissue.min), myocytes length (mm), diameter (mm) and length to diameter ratio, and signs of fibrosis by Masson tricromic staining.Results: Signs of early fibrotic process were observed in heart of Lm and Lf. Zinc deficient rats showed a reduced body and heart weight and cardiac NOS activity.An increase in myocyte length was observed in Lm and Lf, meanwhile the diameter was only decreased in Lm and the ratio length/diameter was elevated in both groups. Zinc deficient rats showed a reduced body and heart weight and cardiac NOS activity.An increase in myocyte length was observed in Lm and Lf, meanwhile the diameter was only decreased in Lm and the ratio length/diameter was elevated in both groups. Signs of early fibrotic process were observed in heart of Lm and Lf. Zinc deficient rats showed a reduced body and heart weight and cardiac NOS activity.An increase in myocyte length was observed in Lm and Lf, meanwhile the diameter was only decreased in Lm and the ratio length/diameter was elevated in both groups.Conclusion: This study suggests that zinc restriction during fetal life induces early cardiac alterations that may permanently modify heart structure and function, in m and f, probably by increasing the number of sarcomeres in series. The decrease of cardiac NOS activity may alter cardiac development and function since NO contributes to regulate apoptotic process and heart contraction and rate. This work demonstrates that zinc deficiency induces cardiac alterations in early period of growth that may contribute to program cardiovascular diseases in adult life.