Context-Dependency of the Relation Between Left Ventricular Mass and Agt Gene Variants

Kuznetsova, T.; Staessen, Jan A.; Reineke, T.; Olszanecka, Agnieszka; Ryabikov, A.; Tikhonoff, Valérie; Casíglia, Edoardo; Kawecka‐Jaszcz, K.; Brand, Eva

doi:10.1097/00004872-200406002-01210

Cited by 8 publications

(17 citation statements)

References 28 publications

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“…In one study, an association analysis using a selected set of single-nucleotide polymorphisms representing the overall haplotypes of AGT gene with AGT levels and hypertension did show that the two distantly related haplotypes À532T/235T and À6G/235M were associated with hypertension but had opposite effects on the serum AGT levels in the two studied populations of African origin which were genetically similar but environmentally diverse. 5 An association between AGT haplotype containing À532T and hypertension was observed among African Americans, which was consistent with previous studies. 4 Perhaps attention should be directed towards target organ damage consequent upon hypertension.…”

supporting

confidence: 92%

“…A family-based study conducted in three populations (Polish, Russian and Italian) reported a positive association between left ventricular mass index (LVMI) and mean wall thickness with the AGT À532T allele in Slavic male offspring but not in Italians. 5 This study is therefore more in agreement with the concept that phenotype-genotype correlations differs in relation to gender and epidemiology, including genetic background and lifestyle. Genetic polymorphisms of RAAS genes could also play a role in arterial stiffness leading to an increased risk of development of lower extremity arterial disease and possibly, other vascular disease.…”

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confidence: 88%

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Hypertension and genes: perspectives from this journal

2007

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supporting

confidence: 92%

supporting

confidence: 88%

Hypertension and genes: perspectives from this journal

2007

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“…This finding is in keeping with other published data on the haplotype structure of the AGT gene. 22,23 Thus, carriers of H2-CA or H3-TA might have an elevated AGT concentration in both plasma and tissues. Our finding that H2-CA or H3-TA carriers had lower PRA is in line with this hypothesis.…”

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confidence: 99%

Arterial properties in relation to genetic variation in α-adducin and the renin–angiotensin system in a White population

et al. 2008

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Earlier studies have demonstrated the interaction between ADD1 and ACE in relation to arterial properties. We investigated whether arterial characteristics might also be related to interactions of ADD1 with other renin-angiotensin system genes. Using a family-based sampling frame, we randomly recruited 1064 Flemish subjects (mean age, 43.6 years; 50.4% women). By means of a wall-tracking ultrasound system, we measured the properties of the carotid, femoral and brachial arteries. In multivariate-adjusted analyses, we assessed the multiple gene effects of ADD1 (Gly460Trp), AGT (C-532T and G-6A) and AT1R (A1166C). In ADD1 Trp allele carriers, but not in ADD1 GlyGly homozygotes (P-value for interaction p0.014), femoral cross-sectional compliance was significantly higher (0.74 vs 0.65 mm 2 kPa À1 ; P ¼ 0.020) in carriers of the AT1R C allele than in AT1R AA homozygotes, with a similar trend for femoral distensibility (11.3 vs 10.2 Â 10 À3 kPa À1 ; P ¼ 0.055). These associations were independent of potential confounding factors, including age. Familybased analyses confirmed these results. Brachial diameter (4.35 vs 4.18 mm) and plasma renin activity (PRA) (0.23 vs 0.14 ng ml À1 h À1 ) were increased (Pp0.005) in AGT CG haplotype homozygotes compared with noncarriers, whereas the opposite was true for brachial distensibility (12.4 vs 14.4 Â 10 À3 kPa À1 ; P ¼ 0.011). There was no interaction between AGT and any other gene in relation to the measured phenotypes. ADD1 and AT1R interactively determine the elastic properties of the femoral artery. There is a single-gene effect of the AGT promoter haplotypes on brachial properties and PRA.

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“…Одно из наиболее крупных исследо-ваний по анализу его влияния на ГЛЖ -семейное ев-ропейское исследование EPOGH (European Project on Genes in Hypertension), в котором обследованы три по-пуляции (польская, русская, итальянская), всего 221 се-мья (384 родителей и 440 детей) [23]. В трех центрах получена зависимость между ММЛЖ и преобладани-ем аллеля А (55,7% против 40,6%), причем зависимость подтверждена только у мужчин.…”

Section: Clinical and Genetic Factors Of Left Ventricular Hypertrophyunclassified

Association of Clinical and Genetic Factors With Left Ventricle Hypertrophy in Arterial Hypertension

Kuznetsova

Gavrilov²,

Rebrikov

et al. 2010

Racionalʹnaâ farmakoterapiâ v kardiologii

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Aim. To evaluate association of clinical and genetic factors with left ventricle hypertrophy (LVH) in patients with arterial hypertension (HT).Materials and methods. 672 patients with HT were involved, aged 50,6 y.o. in average, men 67%. Laboratory assays, ECG, echocardiography were performed. Control group included 184 healthy persons. Genotyping with single-nucleotide substitutions of the endothelial NO synthase (eNOS) Glu298Asp gene, the C242T of the NADPH oxidase p22phox subunit and the angiotensin 2 receptor type 1 А1166С gene was carried out using a polymerase chain reaction (PCR) with evaluating of restriction fragments length polymorphism, while with substitutions of the angiotensinogen М235Т, G(-6)A gene allele-specific PCR "in real time" was applied.Results. LVH was found in 39% of patients. It was more frequent in persons above 50 years old (OR 2,8, р<0,0001), in men (OR 1,43, p=0,035), in HT of degree 2-3 (OR 3,35, р<0,0001), HT duration more than 5 years (OR 2,52, р<0,05), in obesity (OR 1,57, р=0,005) or diabetes (OR 3,33, р<0,0001) presence. At genetic factors evaluation decrease of LVH risk was revealed in persons with the MM polymorphism of the angiotensinogen М235Т gene (OR 0,506, р=0,0187). Association of the MM genotype with LVH risk lowering was more obvious at the young age (OR 0,31, р=0,018). The A allele of the eNOS gene Glu298Asp polymorphism increased risk of LVH development when HT was diagnosed in the young age (OR 1,98, р=0,037) and in women up to 50 years old (OR 2,34, р=0,027). The T allele of the p22phox NADPH oxidase gene С242Т polymorphism correlated with LVH risk reduction in HT patients up to 50 years old (OR 0,6, p=0,01), the C allele -with increase of it (OR 1,66, р=0,01), this influence was more noticeable in women up to 50 years old (T allele -OR 0,21; C allele -OR 4,57, p=0,001). Conclusion. Hypertensive LVH correlates with age, male gender, HT degree and duration, obesity and diabetes mellitus. Genetic factors were less associated with LVH. Цель. Анализ ассоциации клинических и генетических факторов с гипертрофией левого желудочка (ГЛЖ) у пациентов с артериальной гипертонией (АГ). Материал и методы. Обследованы 672 пациента АГ, средний возраст 50,6 лет, мужчин 67%. Выполнялись лабораторные исследования, ЭКГ, эхокардиография. Группу контроля состави-ли 184 человека. Генотипирование по однонуклеотидным заменам Glu298Asp гена эндотелиальной NO синтазы, С242Т субъединицы p22phox NADPH оксидазы и А1166С гена рецептора 1 типа к ангиотензину 2 проводилось методом полимеразной цепной реакции (ПЦР) с анализом полиморфизма длины рестрикционных фрагментов, а по заменам М235Т, G(-6)A гена ангио-тензиногена с помощью аллель-специфичной ПЦР «в реальном времени». Результаты. ГЛЖ диагностирована у 39% больных, чаще в возрасте старше 50 лет (ОШ 2,8, р<0,0001), у мужчин (ОШ 1,43, р=0,035), при наличии 2-3 степени АГ (ОШ 3,35, р<0,0001), давности АГ более 5 лет (ОШ 2,52, p<0,05), при наличии ожирения (ОШ 1,57, р=0,005), сахарного диабета (ОШ 3,33, р<0,0001). При анализе генетических факто...

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Context-Dependency of the Relation Between Left Ventricular Mass and Agt Gene Variants

Cited by 8 publications

References 28 publications

Hypertension and genes: perspectives from this journal

Hypertension and genes: perspectives from this journal

Arterial properties in relation to genetic variation in α-adducin and the renin–angiotensin system in a White population

Association of Clinical and Genetic Factors With Left Ventricle Hypertrophy in Arterial Hypertension

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