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(Hypertension. 2004;43:780.)
© 2004 American Heart Association, Inc.
Scientific Contributions |
From the Department of Epidemiology (K.E.N., K.M.R.), University of North Carolina, Chapel Hill; Washington University School of Medicine (I.B.B.), St. Louis, Mo; Division of Preventive Medicine (A.O.), Department of Medicine, University of Alabama at Birmingham; Cardiovascular Genetics Research Clinic (S.C.H.), Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City; Division of Epidemiology (M.B.M., J.S.P.), University of Minnesota, Minneapolis; and Department of Genetics (J.B., L.A.), Southwest Foundation for Biomedical Research, San Antonio, Tex.
Correspondence to Kari North, Department of Epidemiology, University of North Carolina Chapel Hill, Bank of America Center, 137 E. Franklin St., Suite 306, Chapel Hill, NC 27514. E-mail kari_north{at}unc.edu
Previous analysis in the Hypertension Genetic Epidemiology Network (HyperGEN) of the National Heart Lung and Blood Institute (NHLBI) Family Blood Pressure Program, a multicenter study of genetic and environmental factors related to hypertension, indicated regions of linkage for blood pressure traits together with several coincident regions for phenotypically correlated traits, including systolic blood pressure (SBP) response to a postural challenge and body mass index (BMI). Motivated by these findings and by our desire to better understand the physiology of these traits, we conducted bivariate linkage analysis of postural SBP change and BMI. Sibships in HyperGEN were recruited from 5 field centers in Massachusetts, North Carolina, Minnesota, Utah, and Alabama. All available affected siblings, their parents, and selected nonmedicated offspring were recruited. Among 1636 whites and 1747 blacks, we performed a maximum likelihood bivariate genome scan for quantitative trait loci influencing postural SBP change and BMI, similarly adjusted for race, study center, sex, age, and age-by-sex interactions. Genome scans were performed using SOLAR (version 2.0) and race-specific marker allele frequencies derived from founders. The maximum genome-wide logarithm of odds (LOD) score of 3.2 was detected on chromosome 13 at 24 cM. This marker (D13S493) lies within 20 cM of a marker previously linked to BMI in the Family Heart Study and is substantially higher than the univariate linkage for each trait (LOD scores for BMI and postural SBP change were 2.4 and 0.9, respectively). These findings suggest that a gene(s) on chromosome 13q jointly regulates the SBP response to postural change and BMI.
Key Words: genetics hypotension posture body mass index blood pressure
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