Blood pressure and genetic and biological markers in a pediatric population.

Background: It is universally accepted that atherosclerosis originates in childhood and that high LDL and low HDL serum cholesterol, hypertension and obesity are some of the main risk factors. In the past few years, increasing importance has been attributed to the deleterious effect of reactive oxygen species (ROS) on lipids, on the endothelial lining of arteries, and on the occurrence of cardiovascular disease. The relationship between blood pressure, active renin (AR) and the genetic polymorphism of haptoglobin in a population of adolescents was studied using pro-oxidant status markers, and also using some enzyme systems involved in the antioxidant defense mechanisms of the body. Methods: 51 healthy children, 9 to 12 years of age, were evaluated. The following examinations were performed: nutritional status (weight, height, skinfolds and body mass index) and blood pressure; note was made of any family history of cardiovascular disease. The biological parameters assessed by internationally recommended methods included haptoglobin phenotyping and determination of active renin (AR), the Na /Li + countertransport system (Na + /Li + CTR), antioxidant enzyme systems, metahemoglobin reductase (MetHbRed) and transmembrane reductase (TMR) and indicators of oxidative status, namely activity of plasma epinephrine oxidase (EO) and erythrocytic acid phosphatase (LMW-PTP). Results: The study of the behavior of AB. Na + / Li + CTR. EO and erythrocyte enzymes (MetHbRed, TMR and LMW-PTP) according to haptoglobin genetic phenotypes, to haptoglobin genetic phenotypes, only showed a signific ant difference for ren with lower values for allcle 1 carriers (bomoand heterozygous) (p<0.05). There were no ficant differences in blood pressure as significant differences in blood pressure as regards the haptoglobin genetic phenotypes The analysis of the behavior of the same analysis of the behavior of the biochemical parameters considering a family history of cardiovascular discase (CVD) showed higher values of TMR and lower values of EO in individual with values of EO in individuals with negative family history. L near multiple regression showed some biological (Na + /Li + CTR and showed some biological (Na + /Li + CTR and MetHbRed) and genetic parameters (haptoglobin and family history of and family history of cardiovascular disease) to be stronger determinants of systolic blood pressure. Conclusions: It would appear that there is a tendency for some intermediate biochemical phenotypes to express early on in childhood in individuals with a family history of CVD, which would point to an evident genetic disposition towards this type of pathology.