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Genetic polymorphisms and erythrocyte sodium-lithium countertransport in essential hypertension

Kurt Tournoy UGent, Joris Delanghe UGent, Daniel Duprez UGent, Marc De Buyzere UGent, Ronald Verbeeck UGent, Donald A Vergauwe, Geert Leroux-Roels UGent and Denis Clement UGent (1996) CLINICA CHIMICA ACTA. 255(1). p.39-55
abstract
Erythrocyte sodium-lithium countertransport (SLC) activity is elevated in essential arterial hypertension. With the growing attention to the genetic substrate of disturbed biochemical tests associated with essential arterial hypertension, we were particularly interested in the involvement of key genes for the regulation of SLC, possibly related to the pathophysiology of essential arterial hypertension. Consequently, the aim of the present study was to investigate SLC and its determining factors in essential hypertension. The influence of haptoglobin (Hp)-polymorphism, insertion/deletion polymorphism of angiotensin converting enzyme (ACE-I/D) and MNS blood group system on the regulation of SLC was studied. SLC activity was studied in a cross-sectional case-control study including 90 Caucasians: 60 patients with essential arterial hypertension who had been treated for at least 1 year and 30 normotensive controls. In essential hypertension, the SLC activity is significantly higher (P = 0.00005) than in controls. In normotensive patients, no differences in SLC are observed for the different polymorphisms studied. However, in the hypertensive group, SLC activity is higher (P = 0.003) in Hp 2-1 phenotype and independent of ACE-I/D genotyping and MNS blood group polymorphism. Multifactor analysis of variance in essential hypertension reveals significant (P = 0.001) differences in SLC activity for the presence or absence of Hp 2-1 phenotype and for body weight (P = 0.0003). Multivariate regression analysis shows the same parameters to be independent determining factors of SLC in essential arterial hypertension. No relation is found between SLC activity and target organ damage which includes coronary artery disease, peripheral arterial occlusive disease, left ventricular hypertrophy and cerebrovascular accident. We conclude that erythrocyte SLC activity is elevated despite pressure-lowering therapy. In essential arterial hypertension, individuals of Wp 2-1 phenotype show higher SLC activity than patients of other Hp-types, suggesting genetic heterogeneity of essential arterial hypertension. The presence or absence of Hp 2-1 phenotype is an independent determining factor of SLC activity whereas body weight codetermines SLC activity in essential hypertension.
Please use this url to cite or link to this publication:
author
organization
alternative title
Genetic polymorphisms and erythrocyte sodium-lithium counter-transport in essential hypertension
year
type
journalArticle (original)
publication status
published
subject
keyword
hypertension, genetics Haptoglobin, polymorphism, sodium-lithium countertransport, ESSENTIAL ARTERIAL-HYPERTENSION, NA+-LI+ COUNTERTRANSPORT, BLOOD-PRESSURE, HAPTOGLOBIN, PLASMA, CHOLESTEROL, ASSOCIATION, SENSITIVITY, LINKAGE, MARKER
journal title
CLINICA CHIMICA ACTA
Clin. Chim. Acta
volume
255
issue
1
pages
39 - 55
Web of Science type
Article
ISSN
0009-8981
DOI
10.1016/0009-8981(96)06389-9
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
191021
handle
http://hdl.handle.net/1854/LU-191021
date created
2004-01-14 13:41:00
date last changed
2012-05-15 13:38:43
@article{191021,
  abstract     = {Erythrocyte sodium-lithium countertransport (SLC) activity is elevated in essential arterial hypertension. With the growing attention to the genetic substrate of disturbed biochemical tests associated with essential arterial hypertension, we were particularly interested in the involvement of key genes for the regulation of SLC, possibly related to the pathophysiology of essential arterial hypertension. Consequently, the aim of the present study was to investigate SLC and its determining factors in essential hypertension. The influence of haptoglobin (Hp)-polymorphism, insertion/deletion polymorphism of angiotensin converting enzyme (ACE-I/D) and MNS blood group system on the regulation of SLC was studied. SLC activity was studied in a cross-sectional case-control study including 90 Caucasians: 60 patients with essential arterial hypertension who had been treated for at least 1 year and 30 normotensive controls. In essential hypertension, the SLC activity is significantly higher (P = 0.00005) than in controls. In normotensive patients, no differences in SLC are observed for the different polymorphisms studied. However, in the hypertensive group, SLC activity is higher (P = 0.003) in Hp 2-1 phenotype and independent of ACE-I/D genotyping and MNS blood group polymorphism. Multifactor analysis of variance in essential hypertension reveals significant (P = 0.001) differences in SLC activity for the presence or absence of Hp 2-1 phenotype and for body weight (P = 0.0003). Multivariate regression analysis shows the same parameters to be independent determining factors of SLC in essential arterial hypertension. No relation is found between SLC activity and target organ damage which includes coronary artery disease, peripheral arterial occlusive disease, left ventricular hypertrophy and cerebrovascular accident. We conclude that erythrocyte SLC activity is elevated despite pressure-lowering therapy. In essential arterial hypertension, individuals of Wp 2-1 phenotype show higher SLC activity than patients of other Hp-types, suggesting genetic heterogeneity of essential arterial hypertension. The presence or absence of Hp 2-1 phenotype is an independent determining factor of SLC activity whereas body weight codetermines SLC activity in essential hypertension.},
  author       = {Tournoy, Kurt and Delanghe, Joris and Duprez, Daniel and De Buyzere, Marc and Verbeeck, Ronald and Vergauwe, Donald A and Leroux-Roels, Geert and Clement, Denis},
  issn         = {0009-8981},
  journal      = {CLINICA CHIMICA ACTA},
  keyword      = {hypertension,genetics Haptoglobin,polymorphism,sodium-lithium countertransport,ESSENTIAL ARTERIAL-HYPERTENSION,NA+-LI+ COUNTERTRANSPORT,BLOOD-PRESSURE,HAPTOGLOBIN,PLASMA,CHOLESTEROL,ASSOCIATION,SENSITIVITY,LINKAGE,MARKER},
  language     = {eng},
  number       = {1},
  pages        = {39--55},
  title        = {Genetic polymorphisms and erythrocyte sodium-lithium countertransport in essential hypertension},
  url          = {http://dx.doi.org/10.1016/0009-8981(96)06389-9},
  volume       = {255},
  year         = {1996},
}

Chicago
Tournoy, Kurt, Joris Delanghe, Daniel Duprez, Marc De Buyzere, Ronald Verbeeck, Donald A Vergauwe, Geert Leroux-Roels, and Denis Clement. 1996. “Genetic Polymorphisms and Erythrocyte Sodium-lithium Countertransport in Essential Hypertension.” Clinica Chimica Acta 255 (1): 39–55.
APA
Tournoy, K., Delanghe, J., Duprez, D., De Buyzere, M., Verbeeck, R., Vergauwe, D. A., Leroux-Roels, G., et al. (1996). Genetic polymorphisms and erythrocyte sodium-lithium countertransport in essential hypertension. CLINICA CHIMICA ACTA, 255(1), 39–55.
Vancouver
1.
Tournoy K, Delanghe J, Duprez D, De Buyzere M, Verbeeck R, Vergauwe DA, et al. Genetic polymorphisms and erythrocyte sodium-lithium countertransport in essential hypertension. CLINICA CHIMICA ACTA. 1996;255(1):39–55.
MLA
Tournoy, Kurt, Joris Delanghe, Daniel Duprez, et al. “Genetic Polymorphisms and Erythrocyte Sodium-lithium Countertransport in Essential Hypertension.” CLINICA CHIMICA ACTA 255.1 (1996): 39–55. Print.