| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Hypertension. 1999;33:698-702.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
From the Program for Population Genetics, Harvard School of Public Health (T.N., B.W., Z.W., E.W., J.J.R., X.X.); Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School (T.N., K.L); Division of Biological Sciences, Harvard School of Public Health (T.N., X.X.), Boston, Mass; Anhui MEIZHONG Institute for Biomedical Sciences and Environmental Health, Anhui, China (J.Y., W.C., Z.F., X.X.); The Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School (X.X.); Department of Biostatistics, Harvard School of Public Health (N.L.), Boston, Mass; Max Delbrück Centre for Molecular Medicine, Berlin, Germany (K.L.).
Correspondence and reprint requests to Xiping Xu, MD, FXB-101, Harvard School of Public Health, 665 Huntington Ave, Boston, MA 02115-6096. E-mail xxu{at}ppg.harvard.edu
AbstractThe gene encoding
angiotensinogen (AGT) has been widely
studied as a candidate gene for hypertension. Most studies to date have
relied on case-control analysis to test for an excess of
AGT variants among hypertensive cases compared with
normotensive controls. However, with this design, nothing guarantees
that a positive finding is due to actual allelic association as opposed
to an inappropriate control population. To avoid this difficulty in our
study of essential hypertension in Anqing, China, we tested
AGT variants using the transmission/disequilibrium test,
a procedure that bypasses the need for a control sample by testing for
excessive transmission of a genetic variant from parents heterozygous
for that variant. We analyzed two AGT
polymorphisms, M235T and T174M, which have been associated with
essential hypertension in whites and Japanese, using data on 335
hypertensive subjects from 315 nuclear families and their parents.
Except in the group of subjects younger than 25 years, M235 and T174
were the more frequently transmitted alleles. We found that 194
parents heterozygous for M235T transmitted M235 106 times
(P=0.22) and that 102 parents heterozygous for T174M
transmitted T174 60 times (P=0.09). Stratifying
offspring by gender, M235 and T174 were transmitted 60 of 106 times
(P=0.21) and 44 of 75 times (P=0.17),
respectively, in men, and 46 of 88 times (P=0.75) and 16
of 27 times (P=0.44), respectively, in women. Our
results were also negative in all age groups and for the affected
offspring with blood pressure values
160/95 mm Hg. Thus, this
study provides no evidence that either allele of M235T or T174M
contributes to hypertension in this Chinese population.
Key Words: angiotensinogen hypertension, essential transmission/disequilibrium test
This article has been cited by other articles:
![]() |
S. Oparil, M. A. Zaman, and D. A. Calhoun Pathogenesis of Hypertension Ann Intern Med, November 4, 2003; 139(9): 761 - 776. [Full Text] [PDF] |
||||
![]() |
A. Hassan, P. C. Sham, and H. S. Markus Planning genetic studies in human stroke: Sample size estimates based on family history data Neurology, May 28, 2002; 58(10): 1483 - 1488. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Schmidt, F. Fazekas, G. M. Kostner, C. M. van Duijn, and R. Schmidt Angiotensinogen Gene Promoter Haplotype and Microangiopathy-Related Cerebral Damage : Results of the Austrian Stroke Prevention Study Stroke, February 1, 2001; 32(2): 405 - 412. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Ishikawa, S. Baba, T. Katsuya, N. Iwai, T. Asai, M. Fukuda, S. Takiuchi, Y. Fu, T. Mannami, J. Ogata, et al. T+31C Polymorphism of Angiotensinogen Gene and Essential Hypertension Hypertension, February 1, 2001; 37(2): 281 - 285. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Hassan and H. S. Markus Genetics and ischaemic stroke Brain, September 1, 2000; 123(9): 1784 - 1812. [Abstract] [Full Text] [PDF] |
||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1999 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |