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European Americans ( EA ) have a better antihypertensive response to β‐blockers when compared with African Americans, albeit with some variability. We undertook a genomewide association study to elucidate the underlying genetic determinants in  EA  contributing to this variability in blood pressure ( BP ) response. A discovery  genomewide association study  of change in  BP  post–metoprolol treatment was performed in  EA  participants ( n  = 201) from the Pharmacogenomic Evaluation of Antihypertensive Responses‐2 (PEAR‐2) study and tested for replication in the atenolol‐treated  EA  from  the PEAR study  ( n  = 233). Rs294610 in the   FGD 5 , which encodes for FYVE, RhoGEF and PH Domain Containing 5, ( expression quantitative trait loci  for   FGD 5  in the small intestine) was significantly associated with increased diastolic  BP  response to β‐blockers in the PEAR‐2 study ( P  = 3.41 × 10 −6 , β = −2.70) and replicated ( P  = 0.01, β = −1.17) in  the PEAR study . Post–meta‐analysis of these studies, an additional single nucleotide polymorphism rs45545233 in the   SLC 4A1 , encoding for Solute Carrier Family 4 Member 1, ( expression quantitative trait loci  for dual specificity phosphatase 3 in the artery tibial) was identified that was significantly associated with a poor response to β‐blockers ( P  = 3.43 × 10 −6 , β = 4.57) and was replicated in the atenolol add‐on cohort ( P  = 0.007, β = 4.97). We identified variants in   FGD 5  and   SLC 4A1 , which have been previously cited as candidate genes for hypertension, to be associated with a β‐blocker  BP  response in  EA . Further elucidation is warranted of the underlying mechanisms of these variants and genes by which they influence the  BP  response to β‐blockers.

Genomic Association Analysis Reveals Variants Associated With Blood Pressure Response to Beta‐Blockers in European Americans