The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Angiotensin-converting enzyme gene polymorphism predicts the time-course of blood pressure response to angiotensin converting enzyme inhibition in the AASK trial.
Vibha Bhatnagar; Daniel T O'Connor; Nicholas J Schork; Rany M Salem; Caroline M Nievergelt; Brinda K Rana; Douglas W Smith; George L Bakris; John P Middleton; Keith C Norris; et al. (Profiled Author: Lawrence Appel)
University of California San Diego, La Jolla, USA. email@example.com
Journal of hypertension 2007;25(10):2082-92.
OBJECTIVE: It has yet to be determined whether genotyping at the angiotensin-converting enzyme (ACE) locus is predictive of blood pressure response to an ACE inhibitor. METHODS: Participants from the African American Study of Kidney Disease and Hypertension trial randomized to the ACE inhibitor ramipril (n = 347) were genotyped at three polymorphisms on ACE, just downstream from the ACE insertion/deletion polymorphism (Ins/Del): G12269A, C17888T, and G20037A. Time to reach target mean arterial pressure (</=107 mmHg) was analyzed by genotype and ACE haplotype using Kaplan-Meier survival curves and Cox proportional hazard models. RESULTS: Individuals with a homozygous genotype at G12269A responded significantly faster than those with a heterozygous genotype; the adjusted (average number of medications and baseline mean arterial pressure) hazard ratio (homozygous compared to heterozygous genotype) was 1.86 (95% confidence limits 1.32-3.23; P < 0.001 for G12269A genotype). The adjusted hazard ratio for participants with homozygous ACE haplotypes compared to those heterozygous ACE haplotypes was 1.40 (1.13-1.75; P = 0.003 for haplotype). The ACE genotype effects were specific for ACE inhibition (i.e., not seen among those randomized to a calcium channel blocker), and were independent of population stratification. CONCLUSIONS: African-Americans with a homozygous genotype at G12269A or homozygous ACE haplotypes responded to ramipril significantly faster than those with a heterozygous genotype or heterozygous haplotypes, suggesting that heterosis may be an important determinant of responsiveness to an ACE inhibitor. These associations may be a result of biological activity of this polymorphism, or of linkage disequilibrium with nearby variants such as the ACE Ins/Del, perhaps in the regulation of ACE splicing.
This section shows information related to the publication - computed using the fingerprint of the publication - including related publications, related experts and related grants with fingerprints representing significant amounts of overlap between their fingerprint and this publication. The red dots indicate whether those experts or terms appear within the publication, thereby showing potential and actual connections.
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Jackson T Wright; George Bakris; Tom Greene; Larry Y Agodoa; Lawrence J Appel; Jeanne Charleston; DeAnna Cheek; Janice G Douglas-Baltimore; Jennifer Gassman; Richard Glassock; et al.JAMA : the journal of the American Medical Association 2002;288(19):2421-31.
L Y Agodoa; L Appel; G L Bakris; G Beck; J Bourgoignie; J P Briggs; J Charleston; D Cheek; W Cleveland; J G Douglas; et al.JAMA : the journal of the American Medical Association 2001;285(21):2719-28.
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