Fetal Programming of Hypertension Induced by Moderate Zinc Restriction during Prenatal Life and Lactation: Early Morphological and Functional Alterations in Cardiovascular System in Both Sexes

Background Several studies suggest that metabolic disorders and nutritionimbalance during prenatal life may induce adaptationsthat program cardiovascular diseases and hypertension. Wehave previously shown that moderate zinc restriction duringprenatal life, lactation and/or growth leads to the developmentof hypertension and renal dysfunction in adulthood.ObjectivesTo evaluate the presence of early cardiovascular alterationsin rats exposed to a moderate zinc deficient diet during prenatallife and lactation, and to determine whether there aredifferences between males and females.Material and MethodsFemale Wistar rats received low zinc diet or control diet fromthe beginning of pregnancy up to weaning. Four experimentalgroups were established at birth: males and females born fromlow-diet mothers, and males and females born from controldietmothers. Male and female offspring were sacrificed at6 and 21 days of life to evaluate body weight, heart weight,cardiovascular morphometric parameters and nitric oxidesynthase activity in the cardiovascular system and cardiacoxidative status.ResultsThe insufficient zinc intake during prenatal life and lactationinduced a remodeling process of the cardiomyocytewhich was different in males and females, increased cardiacoxidative stress, produced a hypotrophic remodeling of thethoracic aorta and reduced nitric oxide synthase activity inthe cardiovascular system.ConclusionsThis study shows that zinc deficiency induces cardiovascularabnormalities in early stages of development, which are differentin males and females that may contribute to programmingof diseases in adulthood.Objetivos Evaluar la presencia de alteraciones cardiovasculares tempranas en ratas sometidas a una deficiencia moderada de cinc durante la vida fetal y la lactancia y si existen diferencias respecto del sexo.Material y métodosRatas Wistar hembras recibieron durante la preñez hasta el destete una dieta control o baja en cinc. En el momento del nacimiento se conformaron cuatro grupos experimentales: machos y hembras nacidos de madres bajas y machos y hembras nacidos de madres controles. A los 6 y a los 21 días de vida se sacrificaron y se determinaron el peso corporal, el peso del corazón, parámetros morfométricos cardiovasculares, la actividad de la óxido nítrico sintasa en el sistema cardiovascular y el estado oxidativo cardíaco.ResultadosEl aporte insuficiente de cinc durante la vida fetal y la lactancia indujo un proceso de remodelación del cardiomiocito, diferente en machos que en hembras, un aumento del estrés oxidativo cardíaco, una remodelación hipotrófica de la aorta torácica y una disminución de la actividad de la óxido nítrico sintasa en el sistema cardiovascular.ConclusionesEste trabajo demuestra que la deficiencia de cinc induce alteraciones cardiovasculares, distintas en machos que en hembras, tempranas en el desarrollo, que podrían contribuir a la programación de enfermedades en la vida adulta