title: G-protein beta3 subunit gene (GNB3) polymorphism 825C-->T in patients with hypertensive crisis.
abstract: OBJECTIVE
  The polymorphism 825C-->T in exon 10 of the gene GNB3 encoding the beta3 subunit of heterotrimeric guanine nucleotide binding regulatory proteins (G-proteins) results in a splicing variant (GNB3-s) in which the nucleotides 498-620 of exon 9 are deleted. The T allele has been shown to be overrepresented in patients with essential hypertension. Because GNB3-s may support the development of severe elevation of blood pressure, we hypothesized that GNB3 825C-->T may be present more frequently in patients with hypertensive crisis.
  
  
  METHODS
  Case control study.
  
  
  METHODS
  Department of Emergency Medicine at the University Hospital of Vienna, Vienna, Austria.
  
  
  METHODS
  A total of 174 patients admitted to an emergency department for treatment of hypertensive crisis diagnosed as suffering from essential hypertension.
  
  
  METHODS
  None.
  
  
  RESULTS
  Patients were genotyped for the 825C-->T transition in GNB3. An equal number of age- and gender-matched normotensive, healthy individuals served as the control population. The allele frequency of 825C-->T in the GNB3 gene was 0.310 in patients with hypertensive crisis and 0.342 in the control group. There was no difference in genotype distribution and allele frequency between the patients and the age- and gender-matched control group or between the observed prevalence and the occurrence rate expected from the Hardy-Weinberg principle within each group.
  
  
  CONCLUSIONS
  GNB3 825C-->T is not associated with the phenotype of hypertensive crisis in patients suffering from essential hypertension. Furthermore, our data do not support the concept that the 825C-->T transition in the GNB3 gene is associated with essential hypertension.
authors.affiliation: Department of Laboratory Medicine, University of Vienna, Austria.
authors.forename: H
authors.initials: H
authors.lastname: Buchmayer
authors.forename: G
authors.initials: G
authors.lastname: Sunder-Plassmann
authors.forename: M M
authors.initials: MM
authors.lastname: Hirschl
authors.forename: J
authors.initials: J
authors.lastname: Kletzmayr
authors.forename: C
authors.initials: C
authors.lastname: Woisetschläger
authors.forename: A N
authors.initials: AN
authors.lastname: Laggner
authors.forename: W H
authors.initials: WH
authors.lastname: Hörl
authors.forename: M
authors.initials: M
authors.lastname: Födinger
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D016022:Case-Control Studies; D004630:Emergencies; D005091:Exons; D005260:Female; D019204:GTP-Binding Proteins / Q000235:genetics*; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006801:Humans; D006974:Hypertension, Malignant / Q000175:diagnosis / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011110:Polymorphism, Genetic / Q000235:genetics*; D012307:Risk Factors
chemical_list: D019204:GTP-Binding Proteins