title: Physical activity modifies the associations between genetic variants and hypertension in the Chinese children.
abstract: BACKGROUND
  Childhood hypertension is a complex disease influenced by both genetic and environmental factors. We aimed to examine the effect of interactions of five polymorphisms with physical activity on blood pressure (BP)/hypertension in the Chinese children.
  
  
  RESULTS
  A population-based case-control study was carried out in Beijing of China in 2004, which included 619 hypertensive cases and 2458 normal BP controls. Physical activity information was collected through the use of a validated questionnaire, and five polymorphisms were genotyped using TaqMan. In active group, there was no significant association of five polymorphisms and genetic risk score with systolic/diastolic BP (SBP/DBP) and risk of hypertension (all p > 0.05). In contrast, in inactive group, two polymorphisms and genetic risk score were significantly associated with SBP (rs17249754: β = 1.26, 95% confidence interval (CI) 0.61-1.90, p < 0.001; rs1004467: β = 0.68, 95%CI 0.03-1.32, p = 0.039; genetic risk score: β = 1.54, 95%CI 0.74-2.33, p < 0.001); three polymorphisms and genetic risk score were significantly associated with hypertension (rs17249754: odds ratio (OR) = 1.27, 95%CI 1.08-1.49, p = 0.004; rs1378942: OR = 1.25, 95%CI 1.00-1.57, p = 0.050 (marginally significant); rs16998073: OR = 1.17, 95%CI 1.01-1.37, p = 0.044; genetic risk score: OR = 1.38, 95%CI 1.13-1.68, p = 0.001).
  
  
  CONCLUSIONS
  The present study provides evidence that interactions between recently identified variants and physical activity play important roles in the regulation of BP and development of hypertension. Physical activity should be prescribed for hypertensive children, especially for those with high risk genetic alleles.
authors.affiliation: Department of Maternal and Child Health Care, School of Public Health, Shandong University, Jinan 250012, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Xi
authors.forename: Hong
authors.initials: H
authors.lastname: Cheng
authors.forename: Yue
authors.initials: Y
authors.lastname: Shen
authors.forename: Xiaoyuan
authors.initials: X
authors.lastname: Zhao
authors.forename: Dongqing
authors.initials: D
authors.lastname: Hou
authors.forename: Xingyu
authors.initials: X
authors.lastname: Wang
authors.forename: Jie
authors.initials: J
authors.lastname: Mi
mesh_terms: D000293:Adolescent; D000367:Age Factors; D044466:Asian People / Q000235:genetics*; D001794:Blood Pressure / Q000235:genetics*; D001795:Blood Pressure Determination; D000081247:CSK Tyrosine-Protein Kinase; D016022:Case-Control Studies; D016009:Chi-Square Distribution; D002648:Child; D002681:China / Q000453:epidemiology; D003430:Cross-Sectional Studies; D005260:Female; D051521:Fibroblast Growth Factor 5 / Q000235:genetics; D059647:Gene-Environment Interaction; D020022:Genetic Predisposition to Disease; D006801:Humans; D006973:Hypertension / Q000175:diagnosis / Q000208:ethnology / Q000235:genetics* / Q000503:physiopathology; D016014:Linear Models; D016015:Logistic Models; D008297:Male; D009043:Motor Activity; D015999:Multivariate Analysis; D016017:Odds Ratio; D010641:Phenotype; D053499:Plasma Membrane Calcium-Transporting ATPases / Q000235:genetics; D011110:Polymorphism, Genetic; D017346:Protein Serine-Threonine Kinases / Q000235:genetics; D018570:Risk Assessment; D012307:Risk Factors; D013254:Steroid 17-alpha-Hydroxylase / Q000235:genetics; D011795:Surveys and Questionnaires; D019061:src-Family Kinases / Q000235:genetics
chemical_list: C506952:ATP2B1 protein, human; C496449:FGF5 protein, human; D051521:Fibroblast Growth Factor 5; C501892:CYP17A1 protein, human; D013254:Steroid 17-alpha-Hydroxylase; D000081247:CSK Tyrosine-Protein Kinase; D019061:src-Family Kinases; C000631346:CSK protein, human; D017346:Protein Serine-Threonine Kinases; C486409:STK39 protein, human; D053499:Plasma Membrane Calcium-Transporting ATPases