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Titolo:
Molecular genetics of salt-sensitivity and hypertension
Autore:
Luft, FC;
Indirizzi:
Humboldt Univ, Franz Volhard Clin, D-13122 Berlin, Germany Humboldt Univ Berlin Germany D-13122 lhard Clin, D-13122 Berlin, Germany Humboldt Univ, Charite, Fac Med, Max Delbruck Ctr Mol Med, D-13122 Berlin,Germany Humboldt Univ Berlin Germany D-13122 Ctr Mol Med, D-13122 Berlin,Germany
Titolo Testata:
DRUG METABOLISM AND DISPOSITION
fascicolo: 4, volume: 29, anno: 2001,
pagine: 500 - 504
SICI:
0090-9556(200104)29:4<500:MGOSAH>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
EPITHELIAL SODIUM-CHANNEL; APPARENT MINERALOCORTICOID EXCESS; CONVERTING-ENZYME LOCUS; BLOOD-PRESSURE; BARTTERS-SYNDROME; BETA-SUBUNIT; BETA(2)-ADRENERGIC RECEPTOR; LIDDLES-SYNDROME; 11-BETA-HYDROXYSTEROID DEHYDROGENASE; HYPOKALEMIC ALKALOSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Luft, FC Humboldt Univ, Franz Volhard Clin, Wiltberg Str 50,Campus Buch, D-13122 Berlin, Germany Humboldt Univ Wiltberg Str 50,Campus Buch Berlin Germany D-13122
Citazione:
F.C. Luft, "Molecular genetics of salt-sensitivity and hypertension", DRUG META D, 29(4), 2001, pp. 500-504

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 for glucocorticoid-remediable aldosteronism, Liddle syndrome, and apparent mineralocorticoid excess. Furthermore, a recent gain-of-function mutationhas recently been described in the gene for the mineralocorticoid receptor. These genes have been cloned and their functions elucidated. Other monogenic syndromes are currently being intensively studied. However, in the areaof primary hypertension, the successes have relied on the candidate gene approach. Allelic variants in the genes for angiotensinogen, alpha -adducin,the beta2-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. Recently, an association approach wasemployed to implicate the mineralocorticoid receptor gene in salt-sensitivity. Linkage approaches have been attempted and the beta -subunit of the epithelial sodium channel has been linked to hypertension and to blood pressure as a quantitative trait locus. New approaches are necessary to elucidatesalt-sensitive hypertension. The analysis of multiple genes simultaneouslyin terms of a metabolic control analysis may provide a more promising approach.

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Documento generato il 21/05/18 alle ore 13:01:08