title: Angiotensin converting enzyme gene insertion/deletion polymorphism, angiotensinogen gene polymorphisms, family history of hypertension, and childhood blood pressure.
abstract: Earlier epidemiologic studies have yielded inconsistent results on the extent and timing of the blood pressure (BP) increase in offspring of hypertensive parents. We hypothesized that a familial influence on the BP of the offspring exists from birth on, but becomes significant only later in childhood. We studied the influence of familial occurrence of hypertension on the BP of 3596 children aged 6 to 18 years during a 6-year follow-up. In addition, we examined the possible associations of BP variations with polymorphisms of two candidate genes for hypertension, ie, those coding for the angiotensin converting enzyme (ACE) and those coding for angiotensinogen. A positive family history of hypertension was reflected as the occurrence of higher systolic BP values from the age of 9 years and upward among the females and from the age of 12 years and upward among the males. The mean differences in BP varied from 3.2 to 5.8 mm Hg (systolic) and 2.1 to 5.9 mm Hg (diastolic) between the female offspring of normotensive and hypertensive parents and grandparents. The systolic BP values were significantly higher among females with a hypertensive history in two generations in comparison with females from normotensive families. Among the male offspring of hypertensive and normotensive families, the BP differences were inconsistent. The deletion/deletion males had higher systolic BP values than those with other ACE genotypes. In contrast, variation at the angiotensinogen gene locus was not significantly associated with BP. We conclude that parental history of hypertension is a risk factor for high blood pressure among the offspring from the ages of 9 to 12 years and upward, and hypertension within two generations may enhance this effect. Although the common genetic variation of ACE may influence blood pressure in male children and adolescents, our data do not suggest a role for the common variation of the angiotensinogen gene as a BP regulator during childhood.
authors.affiliation: Department of Pediatrics, University of Oulu, Finland.
authors.forename: L
authors.initials: L
authors.lastname: Taittonen
authors.forename: M
authors.initials: M
authors.lastname: Uhari
authors.forename: K
authors.initials: K
authors.lastname: Kontula
authors.forename: K
authors.initials: K
authors.lastname: Kainulainen
authors.forename: H
authors.initials: H
authors.lastname: Miettinen
authors.forename: J
authors.initials: J
authors.lastname: Turtinen
authors.forename: M
authors.initials: M
authors.lastname: Nuutinen
mesh_terms: D000293:Adolescent; D000328:Adult; D000808:Angiotensinogen / Q000235:genetics*; D001794:Blood Pressure / Q000235:genetics*; D002648:Child; D002675:Child, Preschool; D004247:DNA / Q000032:analysis; D017931:DNA Primers / Q000737:chemistry; D004251:DNA Transposable Elements / Q000235:genetics*; D005260:Female; D005500:Follow-Up Studies; D017353:Gene Deletion; D005815:Genetic Code; D005819:Genetic Markers; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000235:genetics*; D008297:Male; D018598:Minisatellite Repeats; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012189:Retrospective Studies
chemical_list: D017931:DNA Primers; D004251:DNA Transposable Elements; D005819:Genetic Markers; D000808:Angiotensinogen; D004247:DNA; D007703:Peptidyl-Dipeptidase A