title: Beta1-adrenergic receptor gene polymorphisms and response to beta1-adrenergic receptor blockade in patients with essential hypertension.
abstract: BACKGROUND
  Studies suggest that the Ser49Gly and Arg389Gly polymorphisms in the beta1-adrenergic receptor might be of functional importance for the cardiovascular system. Both have been associated with altered receptor activity in vitro, and with hypertension and cardiac failure in vivo.
  
  
  OBJECTIVE
  The aim of this study was to test whether these polymorphisms were associated with the change in heart rate or blood pressure in patients with essential hypertension and left ventricular (LV) hypertrophy treated with the beta1-adrenergic receptor blocker atenolol.
  
  
  METHODS
  Blood pressure and heart rate were measured in 101 hypertensive patients with echocardiographically verified LV hypertrophy, randomized in a double-blind study to treatment with either the beta1-adrenergic receptor blocker atenolol or the angiotensin II type I receptor antagonist irbesartan. Changes in blood pressure and heart rate were evaluated after 12 weeks. Beta1-adrenergic receptor genotyping was performed using polymerase chain reaction and restriction fragment length polymorphism.
  
  
  RESULTS
  We found no significant associations between the changes in the measured variables and either of the two polymorphisms. However, carriers of the 49Gly allele showed a tendency toward a greater reduction in heart rate compared with patients with the Ser/Ser49 genotype (p = 0.06).
  
  
  CONCLUSIONS
  The Ser49Gly and Arg389Gly beta1-adrenergic receptor polymorphisms do not seem to exert a major effect on the changes in heart rate and blood pressure during 12 weeks of treatment with atenolol in patients with essential hypertension and LV hypertrophy.
authors.affiliation: Department of Medical Sciences, Uppsala University, Uppsala, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Karlsson
authors.forename: L
authors.initials: L
authors.lastname: Lind
authors.forename: P
authors.initials: P
authors.lastname: Hallberg
authors.forename: K
authors.initials: K
authors.lastname: Michaëlsson
authors.forename: L
authors.initials: L
authors.lastname: Kurland
authors.forename: T
authors.initials: T
authors.lastname: Kahan
authors.forename: K
authors.initials: K
authors.lastname: Malmqvist
authors.forename: K P
authors.initials: KP
authors.lastname: Ohman
authors.forename: F
authors.initials: F
authors.lastname: Nyström
authors.forename: H
authors.initials: H
authors.lastname: Melhus
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000483:Alleles; D001262:Atenolol / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000235:genetics*
chemical_list: D000319:Adrenergic beta-Antagonists; D011943:Receptors, Adrenergic, beta; D001262:Atenolol