Authors

Ervin R. Fox
J. Hunter Young
Yali Li
Albert W. Dreisbach
Brendan J. Keating, University of Pennsylvania Perelman School of Medicine
Solomon K. Musani
Kiang Liu, Northwestern University Feinberg School of Medicine
Alanna C. Morrison, University of Texas Health Science Center at Houston
Santhi Ganesh, Michigan Medicine
Abdullah Kutlar, Medical College of Georgia
Vasan S. Ramachandran, Boston University Chobanian & Avedisian School of Medicine
Josef F. Polak, Tufts Medical Center
Richard R. Fabsitz, Division of Epidemiology and Clinical Applications
Daniel L. Dries, University of Pennsylvania Perelman School of Medicine
Deborah N. Farlow, Broad Institute
Susan Redline, Case Western Reserve University
Adebowale Adeyemo, National Human Genome Research Institute (NHGRI)
Joel N. Hirschorn, Boston Children's Hospital
Yan V. Sun, University of Michigan School of Public Health
Sharon B. Wyatt, University of Mississippi Medical Center
Alan D. Penman
Walter Palmas, Columbia University
Jerome I. Rotter, Cedars-Sinai Medical Center
Raymond R. Townsend, University of Pennsylvania Perelman School of Medicine
Ayo P. Doumatey, National Human Genome Research Institute (NHGRI)
Bamidele O. Tayo, Stritch School of Medicine
Thomas H. Mosley
Helen N. Lyon, Boston Children's Hospital
Sun J. Kang
Charles N. Rotimi, National Human Genome Research Institute (NHGRI)
Richard S. Cooper, Stritch School of Medicine
Nora Franceschini, UNC Gillings School of Global Public Health
J. David Curb, Pacific Health Research Institute Hawaii

Document Type

Article

Publication Date

6-1-2011

Abstract

The prevalence of hypertension in African Americans (AAs) is higher than in other US groups; yet, few have performed genome-wide association studies (GWASs) in AA. Among people of European descent, GWASs have identified genetic variants at 13 loci that are associated with blood pressure. It is unknown if these variants confer susceptibility in people of African ancestry. Here, we examined genome-wide and candidate gene associations with systolic blood pressure (SBP) and diastolic blood pressure (DBP) using the Candidate Gene Association Resource (CARe) consortium consisting of 8591 AAs. Genotypes included genome-wide singlenucleotide polymorphism (SNP) data utilizing the Affymetrix 6.0 array with imputation to 2.5 million HapMap SNPs and candidate gene SNP data utilizing a 50K cardiovascular gene-centric array (ITMAT-Broad-CARe [IBC] array). For Affymetrix data, the strongest signal for DBP was rs10474346 (P = 3.6 ×10-8) located near GPR98 and ARRDC3. For SBP, the strongest signal was rs2258119 in C21orf91 (P = 4.7 × 10-8). The top IBC association for SBP was rs2012318 (P = 6.4 × 10-6)) near SLC25A42 and for DBP was rs2523586 (P = 1.3 3 10-6) near HLA-B. None of the top variants replicated in additional AA (n 5 11 882) or European-American (n = 69 899) cohorts. We replicated previously reported European-American blood pressure SNPs in our AA samples (SH2B3, P = 0.009; TBX3-TBX5, P = 0.03; and CSK-ULK3, P = 0.0004). These genetic loci represent the best evidence of genetic influences on SBP and DBP in AAs to date. More broadly, this work supports that notion that blood pressure among AAs is a trait with genetic underpinnings but also with significant complexity. The Author 2011. Published by Oxford University Press.

Publication Source (Journal or Book title)

Human Molecular Genetics

First Page

2273

Last Page

2284

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