Association of genetic variation with systolic and diastolic blood pressure among African Americans: the Candidate Gene Association Resource study

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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 single-nucleotide 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 × 10 ⁻⁶) near HLA-B. None of the top variants replicated in additional AA ( n = 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.

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Most cited references 22

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Newly identified loci that influence lipid concentrations and risk of coronary artery disease.

Cristen J Willer, Serena Sanna, Anne U. Jackson … (2008)

To identify genetic variants influencing plasma lipid concentrations, we first used genotype imputation and meta-analysis to combine three genome-wide scans totaling 8,816 individuals and comprising 6,068 individuals specific to our study (1,874 individuals from the FUSION study of type 2 diabetes and 4,184 individuals from the SardiNIA study of aging-associated variables) and 2,758 individuals from the Diabetes Genetics Initiative, reported in a companion study in this issue. We subsequently examined promising signals in 11,569 additional individuals. Overall, we identify strongly associated variants in eleven loci previously implicated in lipid metabolism (ABCA1, the APOA5-APOA4-APOC3-APOA1 and APOE-APOC clusters, APOB, CETP, GCKR, LDLR, LPL, LIPC, LIPG and PCSK9) and also in several newly identified loci (near MVK-MMAB and GALNT2, with variants primarily associated with high-density lipoprotein (HDL) cholesterol; near SORT1, with variants primarily associated with low-density lipoprotein (LDL) cholesterol; near TRIB1, MLXIPL and ANGPTL3, with variants primarily associated with triglycerides; and a locus encompassing several genes near NCAN, with variants strongly associated with both triglycerides and LDL cholesterol). Notably, the 11 independent variants associated with increased LDL cholesterol concentrations in our study also showed increased frequency in a sample of coronary artery disease cases versus controls.

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Trends in hypertension prevalence, awareness, treatment, and control rates in United States adults between 1988-1994 and 1999-2004.

Jeffrey A Cutler, Paul Sorlie, Michael Wolz … (2008)

This study assesses trends in hypertension prevalence, blood pressure distributions and mean levels, and hypertension awareness, treatment, and control among US adults, age >or=18 years, between the third National Health and Nutrition Examination Survey (1988-1994) and the 1999-2004 National Health and Nutrition Examination Survey, a period of approximately 10 years. The age-standardized prevalence rate increased from 24.4% to 28.9% (P<0.001), with the largest increases among non-Hispanic women. Depending on gender and race/ethnicity, from one fifth to four fifths of the increase could be accounted for by increasing body mass index. Among hypertensive persons, there were modest increases in awareness (P=0.04), from 68.5% to 71.8%. The rate for men increased from 61.6% to 69.3% (P=0.001), whereas the rate for women did not change significantly. Rates remained higher for women than for men, although the difference narrowed considerably. Improvements in treatment and control rates were larger: 53.1% to 61.4% and 26.1% to 35.1%, respectively (both P<0.001). The greatest increases occurred among non-Hispanic white men and non-Hispanic black persons, especially men. Mexican American persons showed improvement in treatment and control rates, but these rates remained the lowest among race/ethnic subgroups (47.4% and 24.3%, respectively). Among all of the race/ethnic groups, women continued to have somewhat better awareness, treatment, and control, except for control rates among non-Hispanic white persons, which became higher in men. Differences between non-Hispanic black and white persons in awareness, treatment, and control were small. These divergent trends may translate into disparate trends in cardiovascular disease morbidity and mortality.

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A high-density admixture map for disease gene discovery in african americans.

P Jäger, Jean-Louis Sankalé, J Phair … (2004)

Admixture mapping (also known as "mapping by admixture linkage disequilibrium," or MALD) provides a way of localizing genes that cause disease, in admixed ethnic groups such as African Americans, with approximately 100 times fewer markers than are required for whole-genome haplotype scans. However, it has not been possible to perform powerful scans with admixture mapping because the method requires a dense map of validated markers known to have large frequency differences between Europeans and Africans. To create such a map, we screened through databases containing approximately 450000 single-nucleotide polymorphisms (SNPs) for which frequencies had been estimated in African and European population samples. We experimentally confirmed the frequencies of the most promising SNPs in a multiethnic panel of unrelated samples and identified 3011 as a MALD map (1.2 cM average spacing). We estimate that this map is approximately 70% informative in differentiating African versus European origins of chromosomal segments. This map provides a practical and powerful tool, which is freely available without restriction, for screening for disease genes in African American patient cohorts. The map is especially appropriate for those diseases that differ in incidence between the parental African and European populations.

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Author and article information

Journal

Journal ID (nlm-ta): Hum Mol Genet

Journal ID (publisher-id): hmg

Journal ID (hwp): hmg

Title: Human Molecular Genetics

Publisher: Oxford University Press

ISSN (Print): 0964-6906

ISSN (Electronic): 1460-2083

Publication date (Print): 1 June 2011

Publication date (Electronic): 4 March 2011

Publication date PMC-release: 4 March 2011

Volume: 20

Issue: 11

Pages: 2273-2284

Affiliations

[1 ]Department of Medicine and

[2 ]School of Nursing, simpleUniversity of Mississippi Medical Center , Jackson, MS, USA,

[3 ]Department of Medicine,

[4 ]Department of Epidemiology and

[5 ]Center for Complex Disease Genomics, McKusick-Nathans Institute of Genetic Medicine, simpleJohns Hopkins University School of Medicine , Baltimore, MD, USA,

[6 ]Department of Epidemiology and Biostatistics and

[7 ]Division of Clinical Epidemiology, simpleCase Western Reserve University , Cleveland, OH, USA,

[8 ]The Institute for Translational Medicine and Therapeutics and

[9 ]Department of Medicine, simpleUniversity of Pennsylvania School of Medicine , Philadelphia, PA, USA,

[10 ]Department of Preventive Medicine, simpleNorthwestern University Feinberg School of Medicine , Chicago, IL, USA,

[11 ]Division of Epidemiology, Human Genetics and Environmental Sciences, simpleThe University of Texas at Houston , Houston, TX, USA,

[12 ]Division of Cardiovascular Medicine, simpleUniversity of Michigan Health System , Ann Arbor, MI, USA,

[13 ]simpleMedical College of Georgia , Agusta, GA, USA,

[14 ]Department of Medicine, simpleBoston University School of Medicine , Framingham, MA, USA,

[15 ]Department of Radiology, simpleTufts-New England Medical Center , Boston, MA, USA,

[16 ]Division of Epidemiology and Clinical Applications and

[17 ]Center for Population Studies, simpleNational Heart, Lung, and Blood Institute , Bethesda, MA, USA,

[18 ]simpleBroad Institute of MIT and Harvard , Cambridge, MA, USA,

[19 ]Center for Research on Genomics and Global Health, National Human Genome Research Institute, Bethesda, MA, USA,

[20 ]Department of Genetics, simpleChildren's Hospital Boston , Boston, MA, USA,

[21 ]Department of Epidemiology, simpleUniversity of Michigan School of Public Health , Ann Arbor, MI, USA,

[22 ]Department of Medicine, simpleColumbia University , New York, NY, USA,

[23 ]Medical Genetics Institute, simpleCedars-Sinai Medical Center , Los Angeles, CA, USA,

[24 ]Department of Epidemiology and Preventive Medicine, simpleStritch School of Medicine , simpleLoyola University , Maywood, IL, USA,

[25 ]UNC Gillings School of Global Public Health, simpleThe University of North Carolina at Chapel Hill , Chapel Hill, NC, USA,

[26 ]simplePacific Health Research Institute , Honolulu, HI, USA,

[27 ]Division of Cardiology, simpleGeorge Washington University , Washington, DC, USA,

[28 ]Division of Biology and Medicine, simpleBrown University , Providence, RI, USA,

[29 ]Clinical Pharmacology and The Genome Centre, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, simpleQueen Mary University of London , London, UK and

[30 ]Department of Cardiology, simpleGeneva University Hospital , Geneva, Switzerland

Author notes

[* ]To whom correspondence should be addressed at: Department of Medicine, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216, USA. Tel: +1 6019845630; fax: +1 6019845638; Email: efox@ 123456umc.edu

[†]

The authors wish it to be known that, in their opinion, the first 3 authors should be regarded as joint First Authors.

[‡]

ICBP-GWAS authors are listed in the Appendix, with authors who are also listed above removed.

Article

Publisher ID: ddr092

DOI: 10.1093/hmg/ddr092

PMC ID: 3090190

PubMed ID: 21378095

SO-VID: 36ab4bff-651f-4e97-9d37-9f0f5f92b8b5

License:

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/2.5), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 18 November 2010

Date accepted : 28 February 2011

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Association of genetic variation with systolic and diastolic blood pressure among African Americans: the Candidate Gene Association Resource study

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Most cited references 22

Newly identified loci that influence lipid concentrations and risk of coronary artery disease.

Trends in hypertension prevalence, awareness, treatment, and control rates in United States adults between 1988-1994 and 1999-2004.

A high-density admixture map for disease gene discovery in african americans.

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Cited by 57