IQUIMEFA   05518
INSTITUTO QUIMICA Y METABOLISMO DEL FARMACO
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Early renal alterations are related with hypertension induced by zinc restriction during fetal life and lactation.
Autor/es:
ARRANZ C.; ELESGARAY R.; VEIRAS L; LOPEZ FERRUCCI D; PLODER M; BALASZCZUK A.; COSTA A.; TOMAT A.
Lugar:
Milán , Italia
Reunión:
Congreso; Nineteenth European Meeting of Hypertension.; 2009
Institución organizadora:
European Society of Hypertension
Resumen:
Objectives: Previously, we have shown that moderate zinc deficiency during fetal life, lactation and/or post-weaning growth programs an increase in blood pressures and an impaired renal function in the adult life. These alterations are associated with a reduction in glomerular filtration surface area, an increase in oxidative stress levels, activation of apoptotic and fibrotic processes and a decrease of nitric oxide (NO) system in the kidney of the adult rats. Our objective was to determine if the renal morphological alterations observed in the adult life of zinc deficient rats were already present in early periods of life and to compare the effects in males and females. Methods: Wistar rats received from the beginning of pregnancy up to weaning low (L, 8ppm) or control (C, 30ppm) zinc diet. At day 21 of postnatal life, male (m) and female (f) offspring of each group of mothers were sacrificed to determine the number of glomeruli per kidney by maceration with hydrochloric acid, the total area and the capillary area of cortical and yuxtamedullar glomeruli, signs of renal fibrosis by Masson tricromic staining and the renal NO synthase (NOS) activity with L-(U14C)-arginine. Results: no signs of fibrotic process were observed in glomeruli, tubules and peritubular interstitium of L and C kidneys. No differences in kidney weight were observed between the experimental groups. *vs C: P<0.01. Conclusion: this study suggests that zinc restriction during fetal life and lactation (nephrogenic period) induces early alterations that may permanently modify the structure of kidney, in males and females, by reducing glomeruli number and inducing compensatory hypertrophy in the remaining nephrons. The decrease in renal NO system activity during early period of growth may alter the renal development since NO contributes to regulate apoptotic process, to decrease renal vascular resistance and to increase renal blood flow and glomerular filtration rate during this period. This work demonstrates that zinc deficiency induce renal morphological alterations in early period of growth that may program hypertension and an impaired renal function in adult life.