Journal
CLINICAL PHARMACOLOGY & THERAPEUTICS
Volume 73, Issue 4, Pages 366-371Publisher
MOSBY, INC
DOI: 10.1016/S0009-9236(02)17734-4
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Funding
- NHLBI NIH HHS [U01 HL65962, HL56251, HL04012] Funding Source: Medline
- NIGMS NIH HHS [GM 5MO1-RR00095, U01GM61374] Funding Source: Medline
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Background. A common polymorphism of the beta(1)-adrenergic receptor Arg389Gly markedly affects function in vitro, but little is known about its in vivo significance. Methods and Results: Resting and exercise hemodynamic responses were measured in subjects homozygous for Arg389 (n = 21) or Gly389 (n = 13) alleles before and 3 hours after administration of a beta-blocker, atenolol. Demographic characteristics and atenolol concentrations were similar in the two genotypic groups. Genotype had a marked effect on resting hemodynamic responses to atenolol, with Arg389-homozygous subjects having a larger decrease in resting systolic blood pressure (8.7 +/- 1.3 mm Hg versus 0.2 +/- 1.7 mm Hg, P < .001) and mean arterial blood pressure (7.2 +/- 1.0 mm Hg versus 2.0 1.7 mm Hg, P = .009). Attenuation of exercise-induced hemodynamic responses by atenolol was not affected by genotype. Conclusions. There is reduced sensitivity of Gly389 homozygotes to a beta-adrenergic receptor antagonist, and this polymorphism may be an important determinant of variability in response to P-blockade.
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