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Research Article

Association of the Renin Gene Polymorphism, Three Angiotensinogen Gene Polymorphisms and the Haplotypes with Essential Hypertension in the Mongolian Population

, , , , , , & show all
Pages 293-300 | Received 24 Mar 2009, Accepted 22 May 2009, Published online: 27 Jul 2010
 

Abstract

Renin is a rate-limiting enzyme of the renin-angiotensin system and plays a crucial role in the regulation of blood pressure (BP). Angiotensinogen (AGT) is the precursor of potent vasoactive hormone angiotensin II and the AGT gene has been incriminated as a marker for genetic predisposition to essential hypertension (EH) in some ethnic groups. The purpose of the study is to explore the association of a new genetic marker of renin gene, and AGT gene M235T, A-6G, and A-20C polymorphisms and their haplotypes with EH in the Mongolian population. On the basis of the prevalence survey, 243 hypertensives and 258 normotensives who had no blood relationship with each other were selected as subjects. All the subjects were interviewed with questionnaires and their blood specimens were collected. Renin gene insertion/ deletion (I/D) polymorphism was genotyped by PCR-polyacrylamide gel electrophoresis. AGT gene M235T, A-6G, and A-20C polymorphisms were genotyped by a PCR-restriction fragment length polymorphism and single-strand conformation polymorphism. The frequencies of renin genotype DD and allele D in hypertensives (36.21%, 63.79%, respectively) were significantly higher than those in normotensives (29.84%, 57.17%, respectively, P < 0.05). The odds ratios (OR) of renin genotype ID, DD to renin genotype II on hypertension were 1.98 (OR 95% CI 1.08–3.72) and 2.51 (OR 95% CI 1.33–4.88), respectively. There were no significant differences in the distributions of genotypes and alleles for AGT gene M235T, A-6G, and A-20C polymorphisms and all different haplotypes between the two groups. Renin gene I/D polymorphism is associated with EH, whereas AGT gene M235T, A-6G, and A-20C polymorphisms and the haplotypes are not associated with EH in the Mongolian population.

ACKNOWLEDGMENTS

This study was supported by the National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Tong Liao Center for Disease Control and Prevention, and the Kezuohouqi Center for Disease Control and Prevention. We would like to thank all the participants for their contribution to this work.

Declaration of Interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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