AGT M235T and ACE ID polymorphisms and exercise blood pressure in the HERITAGE Family Study

1  Pennington Biomedical Research Center, Human Genomics Laboratory, Baton Rouge, Louisiana 70808; 2  Physical Activity Sciences Laboratory, Laval University, Ste-Foy, Quebec, Canada G1K 7P4; 3  Division of Biostatistics and Departments of Genetics and Psychiatry, Washington University, School of Me...

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Published inAmerican journal of physiology. Heart and circulatory physiology Vol. 279; no. 1; pp. H368 - H374
Main Authors Rankinen, Tuomo, Gagnon, Jacques, Perusse, Louis, Chagnon, Yvon C, Rice, Treva, Leon, Arthur S, Skinner, James S, Wilmore, Jack H, Rao, D. C, Bouchard, Claude
Format Journal Article
LanguageEnglish
Published United States 01.07.2000
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Summary:1  Pennington Biomedical Research Center, Human Genomics Laboratory, Baton Rouge, Louisiana 70808; 2  Physical Activity Sciences Laboratory, Laval University, Ste-Foy, Quebec, Canada G1K 7P4; 3  Division of Biostatistics and Departments of Genetics and Psychiatry, Washington University, School of Medicine, St. Louis, Missouri 63110-1093; 4  School of Kinesiology and Leisure Studies, University of Minnesota, Minneapolis, Minnesota 55455; 5  Department of Kinesiology, Indiana University, Bloomington, Indiana 11001; and 6  Department of Health and Kinesiology, Texas A & M University, College Station, Texas 77843-4243 We investigated the association between angiotensinogen (AGT) and angiotensin-converting enzyme (ACE) gene polymorphisms and exercise training responses of resting and exercise blood pressure (BP). BP at rest and during submaximal (50 watts) and maximal exercise tests was measured before and after 20 wk of endurance training in 476 sedentary normotensive Caucasian subjects from 99 families. AGT M235T and ACE insertion/deletion polymorphisms were typed with PCR-based methods. Men carrying the AGT MM and MT genotypes showed 3.7 ± 0.6 and 3.2 ± 0.5 (SE) mmHg reductions, respectively, in diastolic BP at 50 watts (DBP 50 ), whereas, in the TT homozygotes, the decrease was 0.4 ± 1.0 mmHg ( P  = 0.016   for trend, adjusted for age, body mass index, and baseline DBP 50 ). Men with the ACE DD genotype showed a slightly greater decrease in DBP 50 (4.4 ± 0.6 mmHg) than the II and ID genotypes (2.8 ±   0.7 and 2.4 ± 0.5 mmHg, respectively, P  = 0.050). Furthermore, a significant ( P  = 0.022) interaction effect between the AGT and ACE genes was noted for DBP 50 ; the AGT TT homozygotes carrying the ACE D allele showed no response to training. Men with the AGT TT genotype had greater ( P  = 0.007) diastolic BP (DBP) response to acute maximal exercise at baseline. However, the difference disappeared after the training period. No associations were found in women. These data suggest that, in men, the genetic variation in the AGT locus modifies the responsiveness of submaximal exercise DBP to endurance training, and interactions between the AGT and ACE loci can alter this response. genetics; exercise training; family study; intervention study; angiotensinogen; angiotensin-converting enzyme
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ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.2000.279.1.h368