This Article Full Text 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 Ishigami, T. Articles by Ishii, M. Search for Related Content PubMed PubMed Citation Articles by Ishigami, T. Articles by Ishii, M.

(Hypertension. 1997;30:1325-1330.)
© 1997 American Heart Association, Inc.

Articles

Essential Hypertension and 5' Upstream Core Promoter Region of Human Angiotensinogen Gene

Tomoaki Ishigami; Satoshi Umemura; Kouichi Tamura; Kiyoshi Hibi; Nobuo Nyui; Minoru Kihara; Machiko Yabana; Yasujiro Watanabe; Yoichi Sumida; Toshihiro Nagahara; Hisao Ochiai; ; Masao Ishii

From the Second Department of Internal Medicine, Yokohama City University School of Medicine, Yokohama, Japan.

Correspondence to Satoshi Umemura, MD, Second Department of Internal Medicine, Yokohama City University University School of Medicine, 3–9, Fukuura, Kanazawa-ku, Yokohama 236, Japan.

Abstract The angiotensinogen (AGT) gene M235T variant is associated with essential hypertension and elevated plasma AGT concentrations, although the underlying mechanisms are unknown. Recent studies have suggested that AGCE 1 (human AGT gene core promoter element 1) located in the 5' upstream core promoter region (position -25 to -1) of the human AGT gene has an important part in the expression of AGT mRNA by binding with transcription factor AGCF 1 (human AGT gene core promoter element binding factor 1), and a mutation at -20 from adenine to cytosine (A-20C) increases the level of expression of this transcript. We therefore examined subjects with this mutation to study the association with increased plasma AGT concentrations and with essential hypertension. One hundred eighty-eight subjects receiving no antihypertensive medication were examined with regard to the correlation between A-20C and plasma AGT concentrations, and 234 subjects were studied with respect to the association between A-20C and essential hypertension. A-20C was determined by polymerase chain reaction–restriction fragment length polymorphism analysis with EcoOR 109I. Multiple regression analysis showed a weak but significant correlation between A-20C and plasma AGT concentrations (P=.047) and essential hypertension (P=.049). The results suggest that A-20C may underlie the increase in plasma AGT concentrations and be involved in the development of essential hypertension.

Key Words: hypertension, essential • core promoter • angiotensinogen • mutation

This article has been cited by other articles:

				T. V. Pereira, A. C.F. Nunes, M. Rudnicki, Y. Yamada, A. C. Pereira, and J. E. Krieger Meta-Analysis of the Association of 4 Angiotensinogen Polymorphisms With Essential Hypertension: A Role Beyond M235T? Hypertension, March 1, 2008; 51(3): 778 - 783. [Abstract] [Full Text] [PDF]

				M. Sugimoto, T. Furuta, N. Shirai, C. Kodaira, M. Nishino, M. Ikuma, H. Sugimura, and A. Hishida Role of angiotensinogen gene polymorphism on Helicobacter pylori infection-related gastric cancer risk in Japanese Carcinogenesis, September 1, 2007; 28(9): 2036 - 2040. [Abstract] [Full Text] [PDF]

				A. A. Sethi, B. G. Nordestgaard, M.-L. M. Gronholdt, R. Steffensen, G. Jensen, and A. Tybjaerg-Hansen Angiotensinogen Single Nucleotide Polymorphisms, Elevated Blood Pressure, and Risk of Cardiovascular Disease Hypertension, June 1, 2003; 41(6): 1202 - 1211. [Abstract] [Full Text] [PDF]

				A. D. Tiago, N. J. Samani, G. P. Candy, R. Brooksbank, E. N. Libhaber, P. Sareli, A. J. Woodiwiss, and G. R. Norton Angiotensinogen Gene Promoter Region Variant Modifies Body Size-Ambulatory Blood Pressure Relations in Hypertension Circulation, September 17, 2002; 106(12): 1483 - 1487. [Abstract] [Full Text] [PDF]

				K. F. Hilgers, C. Delles, R. Veelken, and R. E. Schmieder Angiotensinogen Gene Core Promoter Variants and Non-Modulating Hypertension Hypertension, December 1, 2001; 38(6): 1250 - 1254. [Abstract] [Full Text] [PDF]

				K. Yanai, K. Hirota, K. Taniguchi-Yanai, Y. Shigematsu, Y. Shimamoto, T. Saito, S. Chowdhury, M. Takiguchi, M. Arakawa, Y. Nibu, et al. Regulated Expression of Human Angiotensinogen Gene by Hepatocyte Nuclear Factor 4 and Chicken Ovalbumin Upstream Promoter-Transcription Factor J. Biol. Chem., December 3, 1999; 274(49): 34605 - 34612. [Abstract] [Full Text] [PDF]

				T. Ishigami, K. Tamura, T. Fujita, I. Kobayashi, K. Hibi, M. Kihara, Y. Toya, H. Ochiai, and S. Umemura Angiotensinogen Gene Polymorphism Near Transcription Start Site and Blood Pressure : Role of a T-to-C Transition at Intron I Hypertension, September 1, 1999; 34(3): 430 - 434. [Abstract] [Full Text] [PDF]

				P. Corvol, A. Persu, A.-P. Gimenez-Roqueplo, and X. Jeunemaitre Seven Lessons From Two Candidate Genes in Human Essential Hypertension : Angiotensinogen and Epithelial Sodium Channel Hypertension, June 1, 1999; 33(6): 1324 - 1331. [Abstract] [Full Text] [PDF]

				T. Niu, J. Yang, B. Wang, W. Chen, Z. Wang, N. Laird, E. Wei, Z. Fang, K. Lindpaintner, J. J. Rogus, et al. Angiotensinogen Gene Polymorphisms M235T/T174M : No Excess Transmission to Hypertensive Chinese Hypertension, February 1, 1999; 33(2): 698 - 702. [Abstract] [Full Text] [PDF]

				K. Tamura, S. Umemura, N. Nyui, K. Hibi, T. Ishigami, M. Kihara, Y. Toya, and M. Ishii Activation of angiotensinogen gene in cardiac myocytes by angiotensin II and mechanical stretch Am J Physiol Regulatory Integrative Comp Physiol, July 1, 1998; 275(1): R1 - R9. [Abstract] [Full Text] [PDF]