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Baroreflex sensitivity and variants of the renin angiotensin system genes

JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 2000年第1期35卷 194-200页

作者： Ylitalo, A Airaksinen, KEJ Hautanen, A Kupari, M Carson, M Virolainen, J Savolainen, M Kauma, H Kesäniemi, YA White, PC Huikuri, HV Univ Oulu Dept Med Div Cardiol FIN-90220 Oulu Finland Univ Oulu Dept Internal Med Atherosclerosis Res Grp FIN-90220 Oulu Finland Univ Oulu Bioctr Oulu FIN-90220 Oulu Finland Univ Helsinki Cent Hosp Div Cardiol Helsinki Finland Univ Texas SW Med Ctr Dept Pediat Dallas TX USA

OBJECTIVES Because the renin-angiotensin-aldosterone system (RAS) modifies cardiovascular autonomic regulation, we studied the possible associations between baroreflex sensitivity (BRS) and polymorphism in the RAS genes. BACKGROUND Wide intersubject variability in BRS is not well explained by cardiovascular risk factors or life style, suggesting a genetic component responsible for the variation of BRS. METHODS Baroreflex sensitivity as measured from the overshoot phase of the Valsalva maneuver and genetic polymorphisms were examined in a random sample of 161 women and 154 men aged 41 to 61 years and then in an independent random cohort of 29 men and 37 women aged 36 to 37 years. An insertion/deletion (I/D) polymorphism of angiotensin-converting enzyme (ACE), M235T variants of angiotensinogen (AGT) and two diallelic polymorphisms in the gene encoding aldosterone synthase (CYP11B2), one in the promoter (-344C/T) and the other in the second intron, were identified by polymerase chain reaction. RESULTS In the older population, BRS differed significantly across CYP11B2 genotype groups in women (10.1 +/- 4.5, 8.7 +/- 3.8 and 7.1 +/- 3.2 ms mm Hg-(-1) in genotypes -344TT, CT and CC, respectively, p = 0.003 and 11.1 +/- 4.4, 8.9 +/- 4.1 and 7.5 +/- 3.4 ms mm Hg-(=1) in intron 2 genotypes 1/1, 1/2 and 2/2, respectively, p = 0.002), bur not in men. No comparable associations were found for BRS with the I/D polymorphism of ACE or the M235T variant of AGT. In the younger population, BRS was even more strongly related to the CYP11B2 promoter genotype (p = 0.0003). The association was statistically significant both in men (p = 0.015) and in women (p = 0.03). CONCLUSIONS Common genetic polymorphisms in the aldosterone synthase (CYP11B2) gene is associated with interindividual variation in BRS. (C) 1999 by the American College of Cardiology.

关键词：芬兰疾病遗传易感性/遗传学基因型高血压/遗传学高血压/病理生理学多态现象遗传/遗传学压力感受器/生理学反射异常/遗传学反射异常/生理学肾素-血管紧张素系统/遗传学肾素-血管紧张素系统/生理学成年人老年人女(雌)性人类男(雄)性中年人

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Lack of association polymorphisms and cardiac among five genetic of the renin-angiotensin system hypertrophy in patients with aortic stenosis

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AMERICAN HEART JOURNAL 2001年第4期141卷 671-676页

作者： Ortlepp, JR Breithardt, O Ohme, F Hanrath, P Hoffmann, R Univ Hosp Aachen Med Clin 1 D-52057 Aachen Germany

Background Patients with aortic stenosis (AS) have left ventricular hypertrophy (LVH). it is thought that LVH in these patients is a consequence of chronic left ventricular pressure overload. However, there is only a poor correlation between the degree of AS and the degree of LVH. Genetic polymorphisms of the renin-angiotensin-aldosterone system (RAAS) have been considered to trigger the response of the left ventricle to chronic pressure overload and determine the degree of LVH in patients with AS. Methods One hundred five consecutive patients with symptomatic AS were examined by echocardiography and left heart catheterization to determine the severity of AS and LVH. Five genetic polymorphisms of the RAAS (ACE, AGTR1, AGT, CMA, CYP11 B2) were analyzed in all patients and the results of genetic analysis were correlated to severity of AS and LVH to determine the importance of the polymorphisms for LVH. Results All tested genotypes were in Hardy-Weinberg equilibrium and allele frequencies were similar to other study populations. There was no correlation between the severity of AS and the severity of LVH. There was no association between the five tested genotypes of the RAAS and the severity of AS (mean gradient and area of the aortic valve) or LVH (LV muscle mass). Conclusion We conclude that LVH in patients with AS is not determined by the tested genetic polymorphisms of the RAAS.

关键词：主动脉瓣狭窄/遗传学基因型肥大左心室/遗传学多态现象遗传肾素-血管紧张素系统/遗传学老年人女(雌)性人类男(雄)性中年人

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Influence of gene polymorphisms of the renin-angiotensin system on clinical outcome in heart failure among the Chinese

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AMERICAN HEART JOURNAL 1999年第4期137卷 653-657页

作者： Sanderson, JE Yu, CM Young, RP Shum, IOL Wei, S Arumanayagam, M Woo, KS Chinese Univ Hong Kong Dept Med & Therapeut Prince Wales Hosp 9-F Clin Sci Bldg Shatin NT Peoples R China Chinese Univ Hong Kong Dept Chem Pathol Prince Wales Hosp Shatin NT Peoples R China

Background An association between the DD allele of the angiotensin-converting enzyme gene and a poorer outcome in patients with heart failure has been found in whites. The DD allele frequency is lower in Chinese, but the M235T variant of the angiotensinogen gene is more common in Chinese than whites;it is not known to what extent polymorphisms of the renin-angiotensin system affect clinical status or prognosis in Chinese patients with heart Failure. Methods We assessed the relations among polymorphism of the angiotensin-converting enzyme gene, angiotensinogen M235T (AGT) gene, and angiotensin type I receptor A1166C gene with left ventricular systolic function, left and right ventricular diastolic function, serum angiotensin-converting enzyme, plasma aldosterone and atrial natriuretic peptide levels at presentation, and clinical outcome at 1 year (survival, hospital admissions) in a cohort of Chinese patients with typical systolic heart failure (n = 82). Results We confirmed the low prevalence of the angiotensin-converting DD and the angiotensin type I receptor CC genotypes, and high prevalence of the AGT TT genotype in Chinese subjects compared with whites. There was no relation between the various gene polymorphisms and survival at 1 year assessed by multiple regression or Cox regression survival analysis. The AC variant of the angiotensin type I receptor gene was associated with morbidity over a 1-year period (hospital admissions) and increased baseline aldosterone levels, but none of the other polymorphisms correlated with systolic or diastolic Function, aldosterone or atrial natriuretic peptide levels. By multiple regression for effects on mortality rate, only atrial natriuretic peptide and age were significant. Conclusions In Chinese patients with heart failure, polymorphisms of the renin-angiotensin system do not appear to be related to survival or severity, probably because of the different prevalence of these genotypes in the Chinese. Thus this study illustr

关键词：醛固酮/血液血管紧张素原/遗传学亚洲大陆世系人群/遗传学心钠素/血液队列研究基因频率基因型香港/流行病学肽基二肽酶A/血液肽基二肽酶A/遗传学多态现象遗传患病率受体血管紧张素/遗传学肾素-血管紧张素系统/遗传学存活率分析心室功能障碍左/血液心室功能障碍左/遗传学心室功能障碍右/遗传学女(雌)性人类男(雄)性中年人

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Human-chimpanzee DNA sequence variation in the four major genes of the renin angiotensin system

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GENOMICS 2000年第1期69卷 14-26页

作者： Dufour, C Casane, D Denton, D Wickings, J Corvol, P Jeunemaitre, X Coll France INSERM U36 Chaire Med Expt & Endocrinol Renale F-75005 Paris France Univ Paris 11 UPRESA CNRS 8080 Equipe Phylogenie & Evolut Mol F-91405 Orsay France Univ Melbourne Howard Florey Inst Expt Physiol & Med Parkville Vic 3052 Australia Ctr Int Rech Med Franceville Gabon

The renin angiotensin system (RAS) is involved in blood pressure control and water/sodium metabolism. The genes encoding the proteins of this system are candidate genes for essential hypertension. The RAS involves four main molecules: angiotensinogen, renin, angiotensin I-converting enzyme, and the angiotensin II type 1 receptor (encoded by the genes AGT, REN, DCP1, and AGTR1, respectively). We performed a molecular screening over 17,037 bp of the coding and 5' and 3' untranslated regions of these genes, from three to six common chimpanzees. We identified 44 single-nucleotide polymorphisms (SNPs) in chimpanzee samples, including 18 coding-region SNPs, 5 of which led to an amino acid replacement. We observed common and different features at various sites (synonymous, nonsynonymous, and noncoding) within and between the four chimpanzee genes: (1) the nucleotide diversity at noncoding sites was similar;(2) the nucleotide diversity at nonsynonymous sites was low, probably reflecting purifying selection, except for the AGT gene;(3) the nucleotide diversity at synonymous sites, which was dependent on the G+C content at the third position of the codon, was high, except for the AGTR1 gene. Comparison of the chimpanzee SNPs with those previously reported for humans identified 119 sites with fixed differences (including 62 coding sites, 17 of which resulted in amino acid differences between the species). Analysis of polymorphism within species and divergence between species shed light on the evolutionary constraints on these genes. In particular, comparison of the pattern of mutation at polymorphic and fixed sites between humans and chimpanzees suggested that the high G+C content of the DCP1 gene was maintained by positive selection at its silent sites. Finally, we propose 68 ancestral alleles for the human RAS genes and discuss the implications for their use in future hypertension-susceptibility association studies. (C) 2000 Academic Press.

关键词：血管紧张素原/遗传学 DNA/化学 DNA/遗传学进化分子外显子基因/遗传学内含子分子序列数据突变黑猩猩属肽基二肽酶A/遗传学多态性单核苷酸受体血管紧张素 1型受体血管紧张素 2型受体血管紧张素/遗传学肾素/遗传学肾素-血管紧张素系统/遗传学序列分析 DNA 变异(遗传学) 动物人类

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Angiotensinogen M235T polymorphism is associated with plasma angiotensinogen and cardiovascular disease

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AMERICAN HEART JOURNAL 1999年第4期137卷 698-705页

作者： Winkelmann, BR Russ, AP Nauck, M Klein, B Böhm, BO Maier, V Zotz, R Matheis, G Wolf, A Wieland, H Gross, W Galton, DJ März, W Ludwigshafen Heart Ctr Dept Cardiol Ludwigshafen Germany Univ Frankfurt Dept Med D-6000 Frankfurt Germany Univ Frankfurt Dept Heart Surg D-6000 Frankfurt Germany Univ Frankfurt Dept Biochem D-6000 Frankfurt Germany Univ Freiburg Dept Med Div Clin Chem D-7800 Freiburg Germany Univ Ulm Dept Med Ulm Germany Univ Dusseldorf Inst Blood Transfus & Hemostasiol D-4000 Dusseldorf Germany St Bartholomews Hosp Dept Metab & Genet London England

Background Genes encoding components of the renin-angiotensin system have been associated with elevated blood pressure (BP) and an increased risk of coronary artery disease. To explore the role of the angiotensinogen (AGT) gene in coronary atherosclerosis and thrombosis, we studied the effect of the AGT M235T gene variant on plasma AGT levels and BP in patients with coronary artery disease and in the subgroup of survivors of myocardial infarction as compared with angiographically defined control subjects. Methods and Results This was a case-control study of 301 white male subjects examined at Frankfurt University medical center. Plasma AGT levels increased stepwise according to the number of T235 alleles present (no T235 allele, 14.8 +/- 3.9 nmol/L;1 allele, 15.7 +/- 5.1 nmol/L;2 alleles, 17.3 +/- 4.7 nmol/L;P = .006). In a multivariate model, circulating AGT emerged as the most important predictor of diastolic pressure (P = .001). In addition, AGT M235T gene polymorphism remained a significant predictor of diastolic BP in a multivariate model adjusted for age, body mass index, fasting glucose, apolipoprotein B, presence of coronary artery disease, and treatment with antihypertensive agents (P < .05). Finally, homozygosity for T235 was associated with increased univariate risk of coronary artery disease and myocardial infarction (odds ratio estimates 1.5;95% confidence intervals 1.1 to 2.1, P = .03, and 1.0 to 2,1, P = .05, respectively). Conclusions The significant relations observed between the AGT M235T variant, its protein product, and the cardiovascular disease phenotypes provide evidence for a possible role of elevated circulating AGT in the pathogenesis of coronary artery disease.

关键词：等位基因血管紧张素原/血液血管紧张素原/遗传学血压/遗传学心血管疾病/遗传学病例对照研究冠状动脉血栓形成/遗传学基因频率基因型多元分析心肌梗死/遗传学比值比肽基二肽酶A/血液多态现象遗传肾素-血管紧张素系统/遗传学危险因素人类男(雄)性中年人

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THE RENIN-ANGIOTENSIN SYSTEM - A BIOLOGICAL MACHINE

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ANNALS OF MEDICINE 1992年第2期24卷 113-115页

作者： BERNSTEIN, KE Dept of Pathology and Lab. Medicine Emory University Atlanta GA 30322 United States

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关键词：染色体图 DNA/生物合成基因表达/遗传学高血压/酶学高血压/遗传学肽基二肽酶A/生物合成肾素-血管紧张素系统/遗传学动物人类

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New insights into the renin-angiotensin system and hypertensive renal disease

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Current Hypertension Reports 1999年第2期1卷 187-194页

作者： Fogo, Agnes B. MCN C3310 Department of Pathology Vanderbilt University Nashville TN 37232 United States

The role of the renin-angiotensin system in hypertension and end organ damage has long been recognized. Recent advances in genetic models and newly available pharmacologic tools have allowed dissection of the mechanisms of actions of the renin-angiotensin system in hypertensive kidney disease. The newly cloned AT₂ receptor is now recognized to oppose many of the AT₁ receptor's actions. The renin-angiotensin system is now recognized to be linked to induction of plasminogen activator inhibitor-1 (PAI-1), possibly via the AT₄ receptor, thus promoting both thrombosis and fibrosis. Interactions of the reninangiotensin system with aldosterone and bradykinin may have impact on both blood pressure and tissue injury. The effects of angiotensin 1 converting enzyme inhibitors versus those of the newly available AT₁ receptor antagonists on blood pressure and organ damage are undergoing evaluation in clinical trials. Finally, polymorphisms of genes relevant to the renin-angiotensin system appear to affect response to treatment, although this effect varies in different populations. Copyright © 1999 by Current Science Inc.

关键词：基因表达/生理学基因型高血压/遗传学高血压/病理生理学肾疾病/遗传学肾疾病/病理生理学纤溶酶原激活物抑制物1/遗传学受体血管紧张素/遗传学肾素-血管紧张素系统/遗传学肾素-血管紧张素系统/生理学动物人类

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Transgenic and knockout mice to study the renin-angiotensin system and other interacting vasoactive pathways

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Current Hypertension Reports 2000年第2期2卷 211-216页

作者： Lake-Bruse, Kristy D. Sigmund, Curt D. Department of Internal Medicine and Physiology and Biophysics University of Iowa College of Medicine Iowa City IA 52242 United States

Essential hypertension is an insidious disease in which the afflicted person risks disability and death from myocardial infarction and stroke. Many factors contribute to the development of essential hypertension, including environment, diet, daily stress, and genetics. Although several single gene disorders causing high blood pressure have been identified, the genetics of essential hypertension are much more complicated. The current hypothesis is that a combination of genetic variations in multiple genes may predispose a person to hypertension. Both overexpression and gene inactivation ("knockout" ) have proven useful tools to evaluate the genetics of essential hypertension and to identify pathways regulating blood pressure. Molecular and physiologic evaluations of transgenic and knockout mice carried out over the past 5 years have provided a plethora of information about the mechanisms of blood pressure regulation and the development and maintenance of hypertension. This review focuses on the newer mouse models that have been developed to investigate hypertension with an emphasis on vascular and renal mechanisms, contributed by the renin-angiotensin system, and other pathways intersecting with the renin-angiotensin system. Copyright © 2000 by Current Science Inc.

关键词：血管紧张素Ⅱ/生理学血管紧张素原/遗传学疾病模型动物高血压/遗传学小鼠基因敲除小鼠转基因一氧化氮/代谢肽基二肽酶A/缺乏肽基二肽酶A/遗传学受体多巴胺/生理学受体神经肽/生理学肾素-血管紧张素系统/遗传学肾素-血管紧张素系统/生理学动物人类小鼠

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