Genome-wide multipoint parametric linkage analysis of pulse pressure in large, extended Utah pedigrees

High pulse pressure, a measure of arterial aging, is an important predictor of cardiovascular and general mortality. It has been suggested that the genetic etiology of pulse pressure is the same as systolic blood pressure. We performed a genome-wide, multipoint, parametric linkage analysis in 26 lar...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2003-09, Vol.42 (3), p.322-328
Main Authors: CAMP, Nicola J, HOPKINS, Paul N, HASSTEDT, Sandra J, COON, Hilary, MALHOTRA, Alka, CAWTHON, Richard M, HUNT, Steven C
Format: Article
Language:English
Subjects:
Adolescent
Adult
Biological and medical sciences
Blood Pressure - genetics
Body Mass Index
Cardiology. Vascular system
Child
Chromosome Mapping
Chromosomes, Human, Pair 12 - genetics
Chromosomes, Human, Pair 8 - genetics
Coronary heart disease
Diastole
Female
Genetic Heterogeneity
Genome, Human
Heart
Humans
Hypertension - genetics
Hypertension - physiopathology
Lod Score
Male
Medical sciences
Microsatellite Repeats
Middle Aged
Models, Genetic
Pedigree
Systole
Utah
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Summary:High pulse pressure, a measure of arterial aging, is an important predictor of cardiovascular and general mortality. It has been suggested that the genetic etiology of pulse pressure is the same as systolic blood pressure. We performed a genome-wide, multipoint, parametric linkage analysis in 26 large, extended Utah pedigrees to locate genes affecting pulse pressure. Four parametric models were considered, including dominant and recessive modes of inheritance involving genes for high and low pulse pressure. Linkage analysis revealed 11 regions with a logarithm of the odds (LOD) >1.5, including 2 regions attaining genome-wide suggestive evidence for linkage after accounting for multiple tests. Inspecting pedigree-specific multipoint linkage evidence suggested that these 2 regions localized to 15.7 cM on chromosome 8p (LOD=2.89), between markers D8S136 and D8S1477, and 20.0 cM on chromosome 12q (LOD=2.59), between D12S1300 and D12S2070. Both regions were identified better by pulse pressure compared with equivalent analyses with systolic or diastolic blood pressure. Results for pulse pressure overlapped favorably with those of others for related blood pressure phenotypes and support the hypothesis that genes with pleiotropic effects on blood pressure phenotypes do exist, but that the genetic etiologies are not identical. In conclusion, our results suggest that pulse pressure might be of use for identifying genes involved in blood pressure phenotypes and arterial aging.
ISSN:0194-911X
1524-4563
DOI:10.1161/01.HYP.0000084874.85653.46