![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Vol. 29, Issue 4, 500-504, April 2001
Franz Volhard Clinic and Max Delbrück Center for Molecular
Medicine, Medical Faculty of the Charité, Campus-Buch, Humboldt
University of Berlin, Germany
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 mutation has 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 area of primary
hypertension, the successes have relied on the candidate gene approach.
Allelic variants in the genes for angiotensinogen, 
-adducin, the
2-adrenergic receptor, the G-protein 3-subunit, and the T594M
mutation in the -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 was employed to implicate the mineralocorticoid
receptor gene in salt-sensitivity. Linkage approaches have been
attempted and the -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 elucidate salt-sensitive hypertension. The analysis of multiple genes simultaneously in terms of
a metabolic control analysis may provide a more promising approach.
This article has been cited by other articles:
|
|
 |
|
  B. C. Rossier and L. Schild Epithelial Sodium Channel: Mendelian Versus Essential Hypertension Hypertension, October 1, 2008; 52(4): 595 - 600. [Full Text] [PDF]
|
|
|
|
 |
|
 R. Alikhani-Koupaei, F. Fouladkou, P. Fustier, B. Cenni, A. M. Sharma, H.-C. Deter, B. M. Frey, and F. J. Frey Identification of polymorphisms in the human 11beta-hydroxysteroid dehydrogenase type 2 gene promoter: functional characterization and relevance for salt sensitivity FASEB J, November 1, 2007; 21(13): 3618 - 3628. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. A. Khalil Dietary salt and hypertension: new molecular targets add more spice Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2006; 290(3): R509 - R513. [Full Text] [PDF]
|
|
|
|
 |
|
 P. Meneton, X. Jeunemaitre, H. E. de Wardener, and G. A. Macgregor Links Between Dietary Salt Intake, Renal Salt Handling, Blood Pressure, and Cardiovascular Diseases Physiol Rev, April 1, 2005; 85(2): 679 - 715. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Andersen, L. Wegner, D. P. Jensen, C. Glumer, L. Tarnow, T. Drivsholm, P. Poulsen, S. K. Hansen, E.-M. D. Nielsen, J. Ek, et al. PGC-1{alpha} Gly482Ser Polymorphism Associates With Hypertension Among Danish Whites Hypertension, April 1, 2005; 45(4): 565 - 570. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Bianchi, P. Ferrari, and J. A. Staessen Adducin Polymorphism: Detection and Impact on Hypertension and Related Disorders Hypertension, March 1, 2005; 45(3): 331 - 340. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Rice, T. Rankinen, Y. C. Chagnon, M. A. Province, L. Perusse, A. S. Leon, J. S. Skinner, J. H. Wilmore, C. Bouchard, and D. C. Rao Genomewide Linkage Scan of Resting Blood Pressure: HERITAGE Family Study Hypertension, June 1, 2002; 39(6): 1037 - 1043. [Abstract] [Full Text] [PDF]
|
|
 |
 |
 |
|
 |
 |
 |
