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The ß1‐Adrenergic Receptor Mediates the Pharmacogenetic Interaction of the ACE D Allele and ß‐Blockers
Author(s) -
Ishizawar David C.,
Janosko Karen M.,
Teuteberg Jeffrey J.,
Cadaret Linda M.,
Mathier Michael A.,
McNamara Dennis M.
Publication year - 2008
Publication title -
clinical and translational science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.303
H-Index - 44
eISSN - 1752-8062
pISSN - 1752-8054
DOI - 10.1111/j.1752-8062.2008.00020.x
Subject(s) - pharmacogenetics , allele , pharmacology , medicine , angiotensin receptor blockers , adverse effect , angiotensin converting enzyme , genotype , beta (programming language) , receptor , beta blocker , adrenergic receptor , endocrinology , biology , genetics , gene , heart failure , blood pressure , computer science , programming language
The role of β‐receptor selectivity for the interaction between the angiotensin‐converting enzyme (ACE) insertion/deletion polymorphism and β‐blocker therapy was investigated in 479 subjects with left ventricular dysfunction. Subjects were separated into no β‐blocker, β1 ‐selective, and nonselective β‐blocker treatment groups. The D allele adversely affected transplant‐free survival for subjects not on β‐blockers ( p = 0.004). Treatment with selective β1‐blockers eliminated the impact of the D allele ( p = 0.51) in a manner similar to nonselective β1,2‐blockers ( p = 0.80). Treatment with β1‐blockers was sufficient to eliminate the adverse impact of the ACE D allele, suggesting this pharmacogenetic interaction is mediated through the β1‐receptor.

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