Genetic Epidemiology of Hypertension in African American

Howard University, Washington DC

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Abstract

The goal of this project in genomic research is to contribute to the growing attempts to fill a major void in resources available to the research community for dissecting the pathophysiology of hypertension (HTN) and related complications in African Americans. It is well documented that A experience one of the highest incidence of HTN in the world. Epidemiologic studies have demonstrated the important role of environmental factors including diet (e.g., high salt intake), lifestyle (e.g., lack of physical activity) and psycho-socio stressors (e.g., employment difficulty) in the etiology of HTN. However, a proportion of the total variance remains unexplained. Because of the importance of family history and observed differential susceptibility to HTN, it is now widely accepted that the etiology of HTN is the result of complex interplay of genetics and the environment. Based on an on-going family study, we propose to recruit a population of 350 AA families with 5 or more members (n> 1,750 persons) in Washington, DC. During a clinical exam, we will collect demographic data, measure BP, height, weight, fat mass, fat free mass, waist and hip circumference. Blood will be drawn for assays of physiologic intermediates including components of the renin-angiotensin aldosterone system (RAAS-Angiotensinogen-AGT, angiotensin-converting enzyme aldosterone system (RAAS-Angiotensinogen-AGT, angiotensin-converting enzyme-ACE and aldosterone), endothelin 1, C-reactive protein (CRP), sodium potassium, calcium, albumin, creatinine, glucose, insulin and leptin. Genomic DNA will be extracted. We propose to evaluate the association and linkage between BP, HTN and genes of the RAAS (ACE, AGT and angiotensin II receptor type 1), epithelial sodium channel beta subunit, endothelial nitric oxide synthase, CRP, endothelin 1, and beta2-adrenergic receptor. We will evaluate single nucleotide polymorphisms (SNP) variations in candidate genes and determine if variation in each SNP and in constructed haplotype, explain variations in BP and HTN risk. In addition, DNA will be stored for future application to conduct genome-wide scan with the goal of identifying novel genomic regions in linkage and association with BP and HTN in AA. Identified novel genomic regions may inform our understanding of the etiology of HTN in other human populations.