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Author Notes:

Correspondence to Yan Gong, PhD, Department of Pharmacotherapy and Translational Research and Center for Pharmacogenomics, University of Florida, PO Box 100486, 1600 SW Archer Road, Gainesville, FL 32610-0486, USA. Tel: +1 352 273 6297; fax: +1 352 273 6121; gong@cop.ufl.edu.

The authors would like to acknowledge and thank the valuable contributions of the PEAR, GENRES, and INVEST study participants, support staff, and PEAR study physicians: Frederic Rabari-Oskoui and Dan Rubin.

Conflicts of interest: Y.G., R.M.C., A.L.B., A.B.C., J.G.G., E.B., S.T.T., and J.A.J. received funding from NIH. J.G.G. is a consultant for BoehringerIngelheim. E.B. received honoraria from the Foundation of Rome. Other authors declare no conflicts of interest.

Subjects:

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Peripheral Vascular Disease
  • Cardiovascular System & Cardiology
  • atenolol
  • blood pressure response
  • genome-wide association study
  • pharmacogenomic evaluation of antihypertensive responses
  • pharmacogenomics
  • PTPRD
  • resistant hypertension
  • CORONARY-ARTERY-DISEASE
  • GLOBAL BURDEN
  • IDENTIFY
  • TRIAL

PTPRD gene associated with blood pressure response to atenolol and resistant hypertension

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Journal Title:

Journal of Hypertension

Volume:

Volume 33, Number 11

Publisher:

, Pages 2278-2285

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Objective: The aim of this study is to identify single-nucleotide polymorphisms (SNPs) influencing blood pressure (BP) response to the β-blocker atenolol. Methods: Genome-wide association analysis of BP response to atenolol monotherapy was performed in 233 white participants with uncomplicated hypertension in the pharmacogenomic evaluation of antihypertensive responses study. Forty-two polymorphisms with P less than 10−5 for association with either diastolic or systolic response to atenolol monotherapy were validated in four independent groups of hypertensive individuals (total n = 2114). Results: In whites, two polymorphisms near the gene PTPRD (rs12346562 and rs1104514) were associated with DBP response to atenolol (P = 3.2 × 10−6 and P = 5.9 × 10−6, respectively) with directionally opposite association for response to hydrochlorothiazide in another group of 228 whites (P = 0.0018 and P = 0.00012). A different polymorphism (rs10739150) near PTPRD was associated with response to atenolol in 150 black hypertensive individuals (P = 8.25 ×10−6). rs12346562 had a similar trend in association with response to bisoprolol (a different β-blocker) in 207 Finnish men in the genetics of drug responsiveness in essential hypertension study. In addition, an intronic single-nucleotide polymorphism (rs4742610) in the PTPRD gene was associated with resistant hypertension in whites and Hispanics in the international verapamil SR trandolapril study (meta-analysis P = 3.2 × 10−5). Conclusion: PTPRD was identified as a novel locus potentially associated with BP response to atenolol and resistant hypertension in multiple ethnic groups.

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