This competitive renewal application requests support to continue a study of hypertension in populations of West African origin. During the first cycle 4,000 family members were recruited from Nigeria, Jamaica, and metropolitan Chicago, IL. Epidemiologic and genetic relationships have been demonstrated for angiotensin I-converting enzyme (ACE) and angiotensinogen (AGT). These genetically related populations live in highly contrasting social settings and a major focus of this project is how environment influences the expression of hypertension-related traits. Substantial differences in familial patterns have been identified in comparisons among the three population samples, suggesting gene-environment interactions. In this renewal phase the total sample will be increased to 6,000 family members. To further elucidate the environmental pathways we will conduct a sub-study cross-classifying participants on the major risk determinants (ie, obesity and sodium intake) and examine gene-environment interactions directly. A genome scan will be used in linkage analysis to identify new chromosomal regions of interest. Two new candidate loci (adducin and beta-2 adrenergic receptor) will be examined and association studies will be conducted using single nucleotide polymorphisms. The full range of analytic tools, including segregation, linkage and cladistic analysis, will be used.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
3R01HL053353-04S1
Application #
6356627
Study Section
Epidemiology and Disease Control Subcommittee 2 (EDC)
Project Start
1995-09-30
Project End
2004-07-31
Budget Start
2000-08-01
Budget End
2001-07-31
Support Year
4
Fiscal Year
2000
Total Cost
$67,293
Indirect Cost
Name
Loyola University Chicago
Department
Public Health & Prev Medicine
Type
Schools of Medicine
DUNS #
791277940
City
Maywood
State
IL
Country
United States
Zip Code
60153
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Wang, Ya-Juan; Tayo, Bamidele O; Bandyopadhyay, Anupam et al. (2014) The association of the vanin-1 N131S variant with blood pressure is mediated by endoplasmic reticulum-associated degradation and loss of function. PLoS Genet 10:e1004641

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