Sodium excretion as a modulator of genetic associations with cardiovascular phenotypes in the European Project on Genes in Hypertension.
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.
Kuznetsova
Tatiana
T
Study Coordinating Centre, Hypertension and Cardiovascular Rehabilitation Unit, Department of Molecular and Cardiovascular Research, University of Leuven, Leuven, Belgium.
Staessen
Jan A
JA
Brand
Eva
E
Cwynar
Marcin
M
Stolarz
Katarzyna
K
Thijs
Lutgarde
L
Tikhonoff
Valérie
V
Wojciechowska
Wiktoria
W
Babeanu
Speranta
S
Brand-Herrmann
Stefan-Martin
SM
Casiglia
Edoardo
E
Filipovský
Jan
J
Grodzicki
Tomasz
T
Nikitin
Yuri
Y
Peleska
Jan
J
Struijker-Boudier
Harry
H
Bianchi
Giuseppe
G
Kawecka-Jaszcz
Kalina
K
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
D002148:Calmodulin-Binding Proteins; D019405:Cytochrome P-450 CYP11B2; D010042:Ouabain; D007703:Peptidyl-Dipeptidase A; D044140:Receptor, Angiotensin, Type 1; D012964:Sodium; D000099291:Adducins