title: Sodium excretion as a modulator of genetic associations with cardiovascular phenotypes in the European Project on Genes in Hypertension.
abstract: Hypertension is a chronic age-related disorder, affecting nearly 20% of all adult Europeans. This disease entails debilitating cardiovascular complications and is the leading cause for drug prescriptions in Europeans older than 50 years. Intensive research over the past two decades has so far failed to identify common genetic polymorphisms with a major impact on blood pressure or associated cardiovascular phenotypes, suggesting that multiple genes each with a minor impact, along with gene-gene and gene-environment interactions, play a role. The European Project on Genes in Hypertension (EPOGH) is a large-scale, family-based study in which participants from seven different populations were phenotyped and genotyped according to standardized procedures. This review article summarizes the initial 5-year findings and puts these observations into perspective against other published studies. The EPOGH demonstrated that phenotype-genotype relations strongly depend on host factors such as gender and lifestyle, in particular salt intake as reflected by the 24-h urinary excretion of sodium. The EPOGH therefore highlights the concept that phenotype-genotype relations can only be studied within a defined ecogenetic context.
authors.affiliation: Study Coordinating Centre, Hypertension and Cardiovascular Rehabilitation Unit, Department of Molecular and Cardiovascular Research, University of Leuven, Leuven, Belgium.
authors.forename: Tatiana
authors.initials: T
authors.lastname: Kuznetsova
authors.forename: Jan A
authors.initials: JA
authors.lastname: Staessen
authors.forename: Eva
authors.initials: E
authors.lastname: Brand
authors.forename: Marcin
authors.initials: M
authors.lastname: Cwynar
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Stolarz
authors.forename: Lutgarde
authors.initials: L
authors.lastname: Thijs
authors.forename: Valérie
authors.initials: V
authors.lastname: Tikhonoff
authors.forename: Wiktoria
authors.initials: W
authors.lastname: Wojciechowska
authors.forename: Speranta
authors.initials: S
authors.lastname: Babeanu
authors.forename: Stefan-Martin
authors.initials: SM
authors.lastname: Brand-Herrmann
authors.forename: Edoardo
authors.initials: E
authors.lastname: Casiglia
authors.forename: Jan
authors.initials: J
authors.lastname: Filipovský
authors.forename: Tomasz
authors.initials: T
authors.lastname: Grodzicki
authors.forename: Yuri
authors.initials: Y
authors.lastname: Nikitin
authors.forename: Jan
authors.initials: J
authors.lastname: Peleska
authors.forename: Harry
authors.initials: H
authors.lastname: Struijker-Boudier
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Bianchi
authors.forename: Kalina
authors.initials: K
authors.lastname: Kawecka-Jaszcz
mesh_terms: D001794:Blood Pressure; D002148:Calmodulin-Binding Proteins / Q000235:genetics; D019405:Cytochrome P-450 CYP11B2 / Q000235:genetics; D006339:Heart Rate; D006801:Humans; D006973:Hypertension / Q000235:genetics*; D017379:Hypertrophy, Left Ventricular / Q000235:genetics; D010042:Ouabain / Q000097:blood; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D010641:Phenotype; D011110:Polymorphism, Genetic; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics; D012964:Sodium / Q000652:urine*; D000099291:Adducins
chemical_list: D002148:Calmodulin-Binding Proteins; D019405:Cytochrome P-450 CYP11B2; D010042:Ouabain; D007703:Peptidyl-Dipeptidase A; D044140:Receptor, Angiotensin, Type 1; D012964:Sodium; D000099291:Adducins