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Aldosterone Synthase Promoter Polymorphism and Cardiovascular Phenotypes in a Large, Multiethnic Population-Based Study
  1. James Brian Byrd, MD, MS*,
  2. Richard J. Auchus, MD, PhD*,
  3. Perrin C. White, MD
  1. From the*University of Michigan, Ann Arbor, MI; and †University of Texas Southwestern Medical Center, Dallas, TX.
  1. Received May 5, 2015, and in revised form May 27, 2015.
  2. Accepted for publication May 28, 2015.
  3. Reprints: James Brian Byrd, MD, MS, Room 20-209W, North Campus Research Complex, University of Michigan, 2800 Plymouth Rd, Ann Arbor, MI 48109. E-mail: jbbyrd{at}med.umich.edu.
  4. The Dallas Heart Study was funded by the Donald W. Reynolds Foundation (Las Vegas, NV). Research reported in this publication was supported by the National Center for Advancing Translational Sciences of the National Institutes of Health under award no. UL1TR001105 and by the National Institute of Diabetes and Digestive and Kidney Diseases under award no. RR21DK103183 (to R.J.A.). J.B.B. was supported by the University of Michigan McKay Award, the Michigan Institute for Clinical & Health Research Translational Research Award, and the University of Michigan Cardiovascular Center Inaugural Award.
  5. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Abstract

Background A single-nucleotide polymorphism in the aldosterone synthase gene (CYP11B2) promoter [−344C/T, rs1799998] has been reported to associate with cardiovascular phenotypes.

Methods The Dallas Heart Study is a large, multiethnic cohort with a high prevalence of hypertension. We genotyped 3452 Dallas Heart Study participants for −344C/T. Generalized linear models were used to assess whether variation at −344C/T associated with plasma aldosterone concentration (PAC), systolic and diastolic blood pressure (SBP and DBP), plasma glucose (in persons with no diabetes), HOMA IR (Homeostasis Model Assessment as an Index of Insulin Resistance), and left ventricular (LV) mass indexed to height. Systolic blood pressure and DBP were significantly higher in blacks compared with whites (P < 0.001 for SBP and for DBP) and Hispanics (P < 0.001 for SBP and for DBP). Log-transformed body mass index was also significantly higher in blacks compared with whites (P < 0.001), but not Hispanics (P = 0.10). Log-transformed PAC was higher in whites compared with blacks (P < 0.001), but did not differ significantly in whites compared with Hispanics (P = 0.73). In univariate and multivariable analysis, −344C/T was not significantly associated with PAC within any ethnicity. In univariate and multivariable analysis, −344C/T was not associated with SBP or DBP within any ethnicity. After adjustment for multiple testing, univariate and multivariable analyses revealed no association between −344C/T and plasma glucose in patients with no diabetes, HOMA IR, or LV mass indexed to height.

Conclusions We were unable to reproduce previously reported associations between −344C/T and PAC, blood pressure, plasma glucose, or LV mass. Methodological differences might explain the differences between our findings and those previously reported.

Key Words
  • aldosterone
  • hypertension
  • genetics
  • glucose
  • left ventricular mass

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