ArticleJournal of human hypertension2002
An association of BMI with A (-6) G, M235T and T174M polymorphisms in angiotensinogen gene in essential hypertension.
Article in Journal of human hypertension, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- The Genetic Variants in the Renin-Angiotensin System and the Risk of Heart Failure in Polish Patients.Genes · 2022Article
- Polymorphism in miR-31 and miR-584 binding site in the angiotensinogen gene differentially influences body fat distribution in both sexes.Genes & nutrition · 2015Article
- Association of T174M polymorphism of angiotensinogen gene with essential hypertension: A meta-analysis.Genetics and molecular biology · 2014Article
- Gene-gene interactions in renin-angiotensin-aldosterone system contributes to end-stage renal disease susceptibility in a Han Chinese population.TheScientificWorldJournal · 2014Article
- Variants and haplotypes in angiotensinogen gene are associated with plasmatic angiotensinogen level in Mexican population.The American journal of the medical sciences · 2011Article
- Linkage of angiotensinogen gene polymorphisms with hypertension in a sibling study of Hong Kong Chinese.Journal of hypertension · 2010Article
- Renin-angiotensin system polymorphisms and risk of hypertension: influence of environmental factors.Journal of clinical hypertension (Greenwich, Conn.) · 2008Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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Abstract
The aim of the study was to assess the existence of possible associations among frequent polymorphisms in angiotensinogen genes and some of the risk factors for essential hypertension, especially body mass index (BMI) and smoking. A total of 192 control subjects (aged 45.87 +/- 3.0 years) and 206 patients with the essential hypertension (aged 48.71 +/- 8.42 years) were compared at three angiotensinogen gene polymorphisms by considering BMI and smoking status. No significant differences in genotype and/or allelic distribution for either A (-6) G ATG, M235T or T174M polymorphisms between the hypertensive and control groups were proved. Significantly more hypertensives than control persons with BMI above 25 kg/m(2) were observed (P(corr) = 0.009), independently on sex distribution. A percentage of 44.6% of smokers in the control group vs 46.0% of smokers in the hypertensive groups were found. No significant difference in concurrence of BMI above 25 kg/m(2) and positive smoking status between control and hypertensive subjects was found. Statistically significant differences were found between control and hypertensive subjects when compared distributions of subjects with certain genotypes of the three examined polymorphisms considering BMI (P(corr) = 0.0002 for AA+AG of A (-6) G ATG, P(corr) = 0.01 for CC + CT of T(174)M ATG and P(corr) = 0.01 for MT + TT of M235T ATG). No functional relationship among obesity and the examined polymorphisms in vivo are known. We conclude that a different distribution of BMI could influence the results of analyses of angiotensinogen gene polymorphisms in essential hypertension-control studies.
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