This Article Full Text Full Text (PDF) All Versions of this Article: 43/2/466    most recent 01.HYP.0000111830.36999.94v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kammerer, C. M. Articles by Atwood, L. D. Search for Related Content PubMed PubMed Citation Articles by Kammerer, C. M. Articles by Atwood, L. D. Related Collections ACE/Angiotension receptors Genetics of cardiovascular disease

(Hypertension. 2004;43:466.)
© 2004 American Heart Association, Inc.

Scientific Contribution

Two Quantitative Trait Loci Affect ACE Activities in Mexican-Americans

Candace M. Kammerer; Nicolas Gouin; Paul B. Samollow; Jane F. VandeBerg; James E. Hixson; Shelley A. Cole; Jean W. MacCluer; Larry D. Atwood

From the Graduate School of Public Health (C.M.K.), University of Pittsburgh, Pittsburgh, Pa; the Southwest Foundation for Biomedical Research (N.G., P.B.S., J.F.V.d.B., S.A.C., J.W.M.), San Antonio, Tex; the University of Texas Health Science Center at Houston (J.E.H.); and Boston University School of Medicine (L.D.A.), Boston, Mass.

Correspondence to Candace M. Kammerer, PhD, Associate Professor, University of Pittsburgh Graduate School of Public Health, Department of Human Genetics, 130 DeSoto St, Pittsburgh, PA 15261. E-mail ckammerer{at}hgen.pitt.edu

Angiotensin-converting enzyme (ACE) activity is highly heritable and has been associated with cardiovascular disease. We are studying the effects of genes and environmental factors on hypertension and related phenotypes, such as ACE activity, in Mexican-American families. In the current study, we performed multipoint linkage analysis to search for quantitative trait loci (QTLs) that affect ACE activities on data from 793 individuals from 29 pedigrees from the San Antonio Family Heart Study. As expected, we obtained strong evidence (maximum log of the odds [LOD]=4.57, genomic P=0.003) that a QTL for ACE activity is located on chromosome 17 near the ACE structural locus. We subsequently performed linkage analyses conditional on the effect of this QTL and obtained strong evidence (LOD=3.34) for a second QTL on chromosome 4 near D4S1548. We next incorporated the ACEIns/Del genotypes in our analyses and removed the evidence for the chromosome 17 QTL (maximum LOD=0.60); however, we retained our evidence for the QTL on chromosome 4q. We conclude that the QTL on chromosome 17 is tightly linked to ACE and is in strong disequilibrium with the insertion/deletion polymorphism, which is consistent with other reports. We also have evidence that an additional QTL affects ACE activity. Identification of this additional QTL might lead to alternate means of prophylaxis.

Key Words: ethnic groups • blood pressure • genetics • hypertension, genetic

This article has been cited by other articles:

				G. I. Rice, A. L. Jones, P. J. Grant, A. M. Carter, A. J. Turner, and N. M. Hooper Circulating Activities of Angiotensin-Converting Enzyme, Its Homolog, Angiotensin-Converting Enzyme 2, and Neprilysin in a Family Study Hypertension, November 1, 2006; 48(5): 914 - 920. [Abstract] [Full Text] [PDF]

				F.A. Sayed-Tabatabaei, B.A. Oostra, A. Isaacs, C.M. van Duijn, and J.C.M. Witteman ACE Polymorphisms Circ. Res., May 12, 2006; 98(9): 1123 - 1133. [Abstract] [Full Text] [PDF]

				M. Falchi, T. Andrew, H. Snieder, R. Swaminathan, G. L. Surdulescu, and T. D. Spector Identification of QTLs for serum lipid levels in a female sib-pair cohort: a novel application to improve the power of two-locus linkage analysis Hum. Mol. Genet., October 15, 2005; 14(20): 2971 - 2979. [Abstract] [Full Text] [PDF]