eNOS (endothelial NO synthase) plays a critical role in the development of ventricular remodelling and cardiac hypertrophy. The purpose of the present study was to determine whether three common variants in NOS3 (the eNOS gene) are associated with the risk of LVH [LV (left ventricular) hypertrophy] in patients with essential hypertension. Three NOS3 genetic variants, −T786C (rs2070744), eNOS4a/b and +G894T (rs1799983), were genotyped in two independent case-control studies: the first study consisted of 1061 hypertensive patients with LVH and 1118 hypertensive patients without LVH, and the second sample consisted of 120 patients with LVH and 223 patients without LVH. Echocardiographic measurements were obtained in all of the hypertensive patients. Only the +G894T (E298D) variant of NOS3 was associated with a higher risk of LVH {OR (odds ratio), 1.67 [95% CI (confidence interval), 1.19–2.36]; P<0.01} in the first population, and replicated in the second population [OR, 1.41 (95% CI, 1.01–2.28); P<0.05] in a recessive model. Compared with carriers of the G allele (GT+GG), patients carrying the TT genotype had increased septal wall thickness (16.2%, P<0.01 and 11.7%, P<0.01 respectively), LV posterior wall thickness (8.3%, P<0.01 and 7.1%, P<0.01 respectively), LV mass index (14.0%, P<0.01 and 25.1%, P<0.01 respectively) and relative wall thickness (13.1%, P<0.01 and 16.2%, P<0.01 respectively) in the first and second populations. The results of the present study support that homozygosity for +G894T (E298D) in NOS3 is a genetic risk factor for the development of LVH in patients with hypertension.
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Research Article|
June 15 2009
A common variant of the eNOS gene (E298D) is an independent risk factor for left ventricular hypertrophy in human essential hypertension
Ying Xin;
Ying Xin
*Sino-German Laboratory for Molecular Medicine, Key Laboratory for Clinical Cardiovascular Genetics of Ministry of Education, FuWai Cardiovascular Hospital and Cardiovascular Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
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Xiaodong Song;
Xiaodong Song
*Sino-German Laboratory for Molecular Medicine, Key Laboratory for Clinical Cardiovascular Genetics of Ministry of Education, FuWai Cardiovascular Hospital and Cardiovascular Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
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Hao Xue;
Hao Xue
*Sino-German Laboratory for Molecular Medicine, Key Laboratory for Clinical Cardiovascular Genetics of Ministry of Education, FuWai Cardiovascular Hospital and Cardiovascular Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
†Hypertension Division, Department of Cardiology, FuWai Cardiovascular Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
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Zhe Liu;
Zhe Liu
*Sino-German Laboratory for Molecular Medicine, Key Laboratory for Clinical Cardiovascular Genetics of Ministry of Education, FuWai Cardiovascular Hospital and Cardiovascular Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
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Xiaojian Wang;
Xiaojian Wang
*Sino-German Laboratory for Molecular Medicine, Key Laboratory for Clinical Cardiovascular Genetics of Ministry of Education, FuWai Cardiovascular Hospital and Cardiovascular Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
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Hu Wang;
Hu Wang
*Sino-German Laboratory for Molecular Medicine, Key Laboratory for Clinical Cardiovascular Genetics of Ministry of Education, FuWai Cardiovascular Hospital and Cardiovascular Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
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Kai Sun;
Kai Sun
*Sino-German Laboratory for Molecular Medicine, Key Laboratory for Clinical Cardiovascular Genetics of Ministry of Education, FuWai Cardiovascular Hospital and Cardiovascular Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
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Yongyi Bai;
Yongyi Bai
*Sino-German Laboratory for Molecular Medicine, Key Laboratory for Clinical Cardiovascular Genetics of Ministry of Education, FuWai Cardiovascular Hospital and Cardiovascular Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
†Hypertension Division, Department of Cardiology, FuWai Cardiovascular Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
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Junhao Liu;
Junhao Liu
*Sino-German Laboratory for Molecular Medicine, Key Laboratory for Clinical Cardiovascular Genetics of Ministry of Education, FuWai Cardiovascular Hospital and Cardiovascular Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
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Rutai Hui
*Sino-German Laboratory for Molecular Medicine, Key Laboratory for Clinical Cardiovascular Genetics of Ministry of Education, FuWai Cardiovascular Hospital and Cardiovascular Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
†Hypertension Division, Department of Cardiology, FuWai Cardiovascular Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China
Correspondence: Dr Rutai Hui (email [email protected] or [email protected]).
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Publisher: Portland Press Ltd
Received:
September 17 2008
Revision Received:
December 19 2008
Accepted:
January 08 2009
Accepted Manuscript online:
January 08 2009
Online ISSN: 1470-8736
Print ISSN: 0143-5221
© The Authors Journal compilation © 2009 Biochemical Society
2009
Clin Sci (Lond) (2009) 117 (2): 67–73.
Article history
Received:
September 17 2008
Revision Received:
December 19 2008
Accepted:
January 08 2009
Accepted Manuscript online:
January 08 2009
Citation
Ying Xin, Xiaodong Song, Hao Xue, Zhe Liu, Xiaojian Wang, Hu Wang, Kai Sun, Yongyi Bai, Junhao Liu, Rutai Hui; A common variant of the eNOS gene (E298D) is an independent risk factor for left ventricular hypertrophy in human essential hypertension. Clin Sci (Lond) 1 July 2009; 117 (2): 67–73. doi: https://doi.org/10.1042/CS20080476
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