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Molecular genetic approaches to human hypertension

Item Type:Book Section
Title:Molecular genetic approaches to human hypertension
Creators Name:Luft, F.C.
Abstract:For the past decade, hypertension research has shifted strongly in the direction of molecular genetics. The success stories are the monogenic hypertensive syndromes. Classic linkage analyses have located the responsible genes and three the genes for glucocorticoid-remediable aldosteronism, Liddle syndrome, and apparent mineralocorticoid excess have been cloned and their functions elucidated. Other monogenic syndromes are currently being intensively studied However, in the area of primary hypertension, the successes have relied on the candidate gene approach. Allelic variants in the genes for angiotensinogen, {alpha}-adducin, {beta}–2 adrenergic receptor, the G-protein beta3 subunit, and the T594M mutation in the {beta} subunit of the epithelial sodium channel have been identified; however, the importance of these allelic variants to primary hypertension as a whole is not yet clear. A variant in the angiotensin converting enzyme gene could initially not be convincingly associated with hypertension, but more recent analyses suggest an influence of the deleted allele on blood pressure in men, but apparently not in women. In all likelihood we are dealing with many genes with small effects. Affected sibling pair linkage analyses will probably not be successful in identifying the loci of these genes. To find new genes, novel approaches will be necessary, including searching for quantitative trait loci linked to blood pressure in normotensive persons, haplotype sharing methodology in trios and family units, the use of better study designs, and the investigation of isolated populations.
Title of Book:From Molecules to Men : Molecular Basis of Congenital Cardiovascular Disorders
Page Range:113-125
Official Publication:https://doi.org/10.1007/978-3-642-57724-6_10

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