(Hypertension. 1999;34:4-7.)
© 1999 American Heart Association, Inc.
Scientific Contribution |
From the Department of Medicine, Hypertension Section (J.B., F.S., A.M., I.G., H.G.), Genetics Program (M.N., A.L. DeS., L.F.), Center for Human Genetics (C.T.B.), Department of Neurology (A.L. DeS., L.F.), and Department of Pediatrics (C.T.B.), Boston University School of Medicine, Boston, Mass; Department of Internal Medicine, Hypertension Section, University of Texas Medical Branch, Galveston, Tex (C.L., F.E.); and Department of Epidemiology and Biostatistics (M.N., A.L. DeS., L.F.), Boston University School of Public Health, Boston, Mass.
Correspondence to Haralambos Gavras, MD, Hypertension Section, W508, Boston University School of Medicine, 715 Albany St, Boston, MA 02118. E-mail hgavras{at}bu.edu
AbstractSeveral clinical and animal studies indicate that essential hypertension is inherited as a multifactorial trait with a significant genetic and environmental component. In the stroke-prone spontaneously hypertensive rat model, investigators have found evidence for linkage to blood pressure regulatory genes (quantitative trait loci) on rat chromosomes 2, 10, and X. In 1 human study of French and UK sib pairs, evidence for linkage has been reported to human chromosome 17q, the syntenic region of the rat chromosome 10 quantitative trait loci (QTL). Our study confirms this linkage (P=0.0005) and refines the location of the blood pressure QTL.
Key Words: hypertension, essential linkage chromosome 17 blood pressure obesity
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