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1.
M235T基因多态性对血压影响的研究   总被引:4,自引:0,他引:4  
叶琼  吴可贵 《高血压杂志》1999,7(4):317-319
目的:研究血管紧张素原基因(AGT)第二外显子M235T等位基因的多态性与高血压之间的关系。方法:应用多聚酶链反应(PCR)结合限制性酶切方法对105例健康体检者与102例原发性高血压(EH)患者进行基因突变的检测。结果:⑴EH患者T235等位基因频率(0.445)高于对照组(0.323),P〈0.05。在男性EH患者与男性对照组中差异更为明显(P〈0.01);⑵在有家族史的EH患者中,M235T  相似文献   

2.
血管紧张素原基因M235T分子变异与原发性高血压的关系   总被引:3,自引:0,他引:3  
目的:探讨血管紧张素原(AGT)基因M235T分子变异与中国人原发性高血压的关系。  方法:对89 例原发性高血压(原发性高血压组)及91 例正常者(正常对照组)用多聚酶链式反应法及限制性片段长度多态性技术对AGT基因M235T多态性进行了检测。  结果:原发性高血压组T等位基因频率0.80,TT基因型频率0.67,与正常对照组(0.66,0.43)比较有显著性差异,(P= 0.023,P= 0.004);TT基因型较MT+ MM 基因型对原发性高血压的比值比为2.76(95% 可信区间为1.50~5.06,P= 0.001)。  结论:AGT基因TT基因型可能与中国人群原发性高血压发病有关联。  相似文献   

3.
老年痴呆患者apoE基因型分布   总被引:17,自引:0,他引:17  
目的观察中国老年痴呆患者apoE基因型的分布,初步探讨apoE在老年痴呆发病中的作用。方法应用聚合酶链式反应(PCR)对35例健康人、23例多梗塞性痴呆(MID)及17例老年性痴呆(AD)患者进行apoE基因多态性分析,测定血清胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、载脂蛋白AⅠ(apoAⅠ)、载脂蛋白B(apoB)和载脂蛋白E(apoE)的浓度。结果AD组与健康对照组在apoE基因频率及等位基因频率分布上的差异有显著性(χ2=11.5,P<0.05;χ2=16.2,P<0.01);MID组与健康对照组间差异无显著性(P>0.05);应用Woolf公式计算,发现apoEε4等位基因与AD之间有显著性关联(χ2=7.7,P<0.01),相关危险度(RR)=3.0。AD组血清apoE水平显著高于对照组(P<0.05),而TC、LDL-C、apoAⅠ、apoB显著低于对照组(P<0.05)。结论结果提示apoEε4等位基因与老年性痴呆有显著性关联,apoEε4可能是AD发病的危险因素。  相似文献   

4.
目的观察老年男性冠心病患者血清硫酸脱氢表雄酮(DHEA-S)含量变化,探讨其与睾酮(T)、胰岛素(INS)、血糖(Glu)、甘油三酯(TG)、总胆固醇(TC)、载脂蛋白B(apoB)及年龄的相关性。方法用放免法测定69例老年男性冠心病患者血清DHEA-S含量,并与35例年龄匹配的男性健康人对照。结果冠心病组DHEA-S含量(2.96±1.80μmol/L)显著低于对照组(4.06±1.76μmol/L,P<0.01),病情重组(2.44±1.36μmol/L)又明显低于病情轻组(3.32±2.12μmol/L,P<0.05);冠心病组DHEA-S含量与年龄呈负相关(r=-0.3054,P<0.01),对照组两者也呈负相关(r=-0.3615,P<0.05);冠心病患者DHEA-S降低与空腹血清INS、TG及apoB增高均呈负相关(分别为r=-0.3297、-0.2519及-0.2413,P<0.01或0.05)。结论老年男性冠心病患者血清DHEA-S含量降低,并与冠心病某些危险因素如老年、高胰岛素血症、高甘油三酯血症、血清apoB高值相关,但其确切的发病机理有待深入研究。  相似文献   

5.
对≥60岁的男性Ⅱ型糖尿病(Ⅱ-DM)患者及合并冠心病患者各50例进行研究,测定其血清T、E2、血糖(GLU)、TC、TG水平。结果:男性Ⅱ-DM及合并冠心病患者血清T低于健康对照组(P<0.05和P<0.01),血清E2也有下降趋势(P>0.05),E2/T比值则高于对照组(P>0.05);相关分析显示T与GLU、TC、TG均呈负相关(P<0.01),而E2则似乎与GLU、TC、TG无明显相关性,GLU与TC、TG呈正相关(P<0.01)。结论:Ⅱ-DM及冠心病患者均存在性激素改变,并与血糖、血酯一起构成影响糖尿病、冠心病的不利因素。  相似文献   

6.
Graves''''病患者下丘脑-垂体-性腺轴功能的变化   总被引:6,自引:0,他引:6  
目的探讨Graves’病(GD)患者下丘脑垂体性腺轴功能的变化。方法对50例GD患者评价性功能,用放免法测定黄体生成素(LH)、卵泡刺激素(FSH)、总睾酮(TT)、游离睾酮(FT)、雌二醇(E2)、并进行黄体生成素释放激素(LHRH)兴奋试验。结果治疗前男女GD患者LH、FSH均高于正常组(P<0.05),LHRH兴奋试验反应增强。男性GD患者TT高于正常组(P<0.05),FT则低于正常组(P<0.05),已婚者性功能障碍者占42.8%。女性GD患者E2较正常组高(P<0.01),月经紊乱者占75%,已婚者性功能障碍57.1%。治疗后上述改变随着甲状腺功能正常而恢复正常。结论GD患者存在下丘脑垂体性腺轴功能紊乱,属可逆性的。  相似文献   

7.
研究中国汉族人血管紧张素 I I的 I型受体( A T1 R) A1166 C 基因多态性与原发性高血压的关系。 方法:测定120 例汉族原发性高血压病人和 86 个汉族正常人的血压、体重指数、空腹血糖及血胆固醇和甘油三酯浓度。用盐析法提取外周血白细胞 D N A,用 P C R加上限制性酶切方法检测 A T1 R的 1166 位基因突变。 结果:高血压组除收缩压、舒张压显著高于对照组外,其它临床指标如体重指数、空腹血糖及血脂水平两组间无显著差异; E H 患者 A T1 R 基因 A C基因型频率比正常对照组 A C基因型频率高(0.181 vs 0.058, P< 0.01), C1166 等位基因频率 E H 组高于正常对照组(0.091 vs 0.029, P< 0.05);两组中均未发现 C C纯合子基因型。 结论:在中国汉族人群中, A C基因型与原发性高血压有关, C等位基因可能是一个高血压的易感基因。  相似文献   

8.
血管紧张素原基因多态性与高血压关系的研究   总被引:9,自引:0,他引:9  
目的研究中国人血管紧张素原基因多态性与原发性高血压的关系。方法应用聚合酶链反应对天津地区112例正常人及131例高血压患者AGT基因235位点限制酶切片段长度多态性进行检测。结果AGT基因235位点有三种基因型为TT、TC、CC,其中CC基因型与高血压发病相关,高血压组C基因频率高于对照组(P=0.032)。结论CC基因型与C等位基因可作为高血压易感性的指标  相似文献   

9.
目的 研究血管紧张素原(AGT)基因M235T多态性对NIDDM患者发生高血压的影响。方法 用限制性普分析法检查AGT基因M235T多态性M235和T235的频率和TT、TM和MM基因型在正常对照组(68例)、糖悄病非高血压组(104例)和糖尿病高血压组(87例)中的分布,并检查各基因型对实验对象血压水平的影响。结果 糖尿病高血压组患者AGT基因M235T多态性T235的频率明显高于对照组和糖尿病  相似文献   

10.
目的:探讨载脂蛋白E(apoE)基因多态性在冠心病(CHD)发生发展中的作用及其对血脂质、脂蛋白水平的影响。方法:应用聚合酶链反应技术和遗传学方法,测定93 例CHD患者和94例正常对照者的apoE基因型;按常规方法测定血浆脂质、脂蛋白水平。结果:共发现5 种apoE基因型,分别为E3/3、E3/2、E4/3、E4/2和E4/4。CHD组apoE4/3 基因型和ε4 等位基因频率及总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)均显著高于对照组(均P< 0.01),apoAI的水平高于对照组(P< 0.05),其他血脂指标无显著性差异( P> 0.05)。在CHD组各亚型之间,TC、LDL-C和apoAI水平之间存在显著性差异(P< 0.05)。结论:apoEε4 等位基因是CHD重要的遗传易患因素,apoE基因多态性亦影响血TC、LDL-C和apoAI水平。  相似文献   

11.
AT_1R基因多态性对血压的影响   总被引:1,自引:0,他引:1  
目的 检测血管紧张素Ⅱ的Ⅰ型受体(AT_1R)C1166等位基因在正常人和原发性高血压(EH)患者中的频率,并研究中国汉族人AT_1R基因多态性与原发性高血压的关系.方法 测定120例汉族原发性高血压病人和86个汉族正常人的血压、体重指数、空腹血糖及血胆固醇和甘油三酯浓度.用盐析法提取外周血白细胞DNA,用PCR加上限制性酶切方法检测AT_1R的C1166位基因突变.结果 高血压组除收缩压、舒张压显著高于对照组外,其它临床指标如体重指数、空腹血糖及血脂水平两组间无显著差异;EH患者AT_1R基因AC基因型频率比正常对照组高(0.081vs 0.058,P<0.01),C1166等位基因频率EH组高于正常对照组(0.091vs 0.029,P<0.05);两组中均未发现CC纯合子基因型;进行性别分组后,发现在女性EH患者C1166等位基因频率高于女性正常对照组(0.125 vs 0. 031,P<0.05),在男性EH患者C166频率与男性正常对照组无显著差异(0.072vs O.028,P>0.05);将EH组分为有、无高血压家族史两组,发现有高血压家族史的EH患者C1166频率高于无家族史EH患者(0.123 vs 0.035,P<0.05).结论 在中国汉族人群中,AT_1R基因多态性与原发性高血压有关;C1166等位基因可能是一个高血压的易感基因,并与有家族史的原发性高血压以及女性高血压病密切相关.  相似文献   

12.
AGT基因M235T多态同哈萨克族高血压病的关联分析   总被引:5,自引:0,他引:5       下载免费PDF全文
目的探讨新疆哈萨克族血管紧张素原(angiotensinogen,AGT)基因第二外显子(M235T)多态性同高血压病(essential hypertension,EH)的关系。方法4次高血压流行病学调查采集新疆巴里坤哈萨克族EH组278例,正常血压(norm altensive,NT)组220例。测定EH患者和NT者体质量指数(BM I)、空腹血糖、血浆胆固醇、甘油三酯。用MS-PCR法(mutagen ically separated polym erase chain reaction techn ique)检测AGT基因M235T多态性。结果M235T多态性符合Hardy-W e inberg平衡。MT、TT、MM基因型分布频率在EH组及NT组分别为32.7%,62.6%,4.7%;38.2%,51.8%,10.0%。T等位基因频率分别为79.0%及70.9%。M235T基因型频率(P<0.05)及等位基因频率(P<0.01)分布在EH组及NT组均有显著性差异。T等位基因携带者OR值为非T等位基因携带者OR值的2.3倍(95%C I 1.14.6;P<0.05)。对未治疗的EH者在不同基因型间进行比较,未发现MT、MM、TT基因型间收缩压、舒张压、体质量指数、血糖、血脂水平有显著性差异。结论AGT基因M235T可能同新疆哈萨克族高血压病发病相关。  相似文献   

13.
Liu J  Lu FH  Wen PE  Jin SK  Wu F  Zhao YX  Liu ZD  Sun SW 《中华心血管病杂志》2005,33(11):1010-1013
目的探讨研究样本中的性别因素对原发性高血压(EH)候选基因研究结果的影响。方法应用聚合酶链反应这一分子生物学研究方法,分析EH组患者及正常血压对照组(两组中男性女性人数相等)人群血管紧张素转换酶(ACE)基因插入/缺失(I/D)多态性,进而探讨性别比例对该类研究结论的可能影响。结果男性EH组DD基因型频率显著高于男性对照组(x^2=6.98,P=0.004),D等位基因频率在男性EH组亦较男性对照组显著增高(x^2=6.87,P=0.009),而ID和II基因型频率在男性EH组和男性对照组间差异无统计学意义(P〉0.05)。女性EH组与女性对照组比较,各基因型和等位基因频率分布差异均无统计学意义(P〉0.05);男性EH组中的DD基因型分布比例与女性EH组中的DD基因型分布比例相比有显著统计学意义(x^2=4.06,P=0.044)。此外,EH组中男性DD型者的收缩压及脉压水平均显著高于ID型和II型者(P均〈0.05),但舒张压在3种基因型间差异无统计学意义(P〉0.05)。同时,EH组II、ID基因型的男性的收缩压、舒张压、脉压差异均无统计学意义(P〉0.05)。女性患者中,各基因型间收缩压、舒张压及脉压的水平差异均无统计学意义(P〉0.05)。结论男性中的DD基因型成员与EH(尤其在收缩压、脉压)的关联可能比男性中的II、ID基因型以及所有的女性更为密切。性别可能作为一个混杂因素,对包括ACE基因I/D多态性在内的诸多EH候选基因与EH的相关性研究的结论产生影响。  相似文献   

14.
Genetic factors play very important role in the pathogenesis of essential hypertension. Angiotensinogen gene is one of the candidate genes in the research concerning genetic background of elevated blood pressure. The aim of this work was to assess an association of M235T polymorphism in human angiotensinogen gene with essential hypertension in Polish population. 250 patients with essential hypertension and 150 normotensives were involved in the study. M235T polymorphism was detected using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) methods. Polymorphic allele and genotypes frequencies did not differ between hypertensive and normotensive groups. However T allele and TT genotype frequency among hypertensive men was higher than in normotensive men. The difference is statistically significant. T allele and TT genotype occurred more frequently in hypertensives with positive family history of essential hypertension. The difference between hypertensive men with positive family history and normotensive men was even more significant. This results are similar to those already published by other authors concerning Caucasian populations and indicate that angiotensinogen gene is involved in the determination of at least some cases of essential hypertension.  相似文献   

15.
目的 探讨肾素 血管紧张素系统 (RAS)基因多态性与原发性高血压左心室肥厚 (EH LVH)的相关性以及在EH LVH产生中的多基因协同作用。方法 对 10 9例原发性高血压病 (EH)患者 ,采用聚合酶链反应 (PCR)以及聚合酶链反应 限制性片段长度多态性方法检测血液白细胞染色体DNA中血管紧张素转换酶 [ACE(I D) ]、血管紧张素原 [AGT(M2 35T) ]和血管紧张素Ⅱ 1型受体 [AT1 R(A116 6C) ]基因多态性 ;利用超声心动图检测左心室质量 (LVM)并计算左心室质量指数 (LVMI)。结果 ACE(I D)基因多态性D等位基因频率在EH LVH组中明显增高 (χ2 =4 .6 9,P=0 .0 30 ) ,男性EH患者中 ,ACE(I D)基因型构成比与LVH有关联 (χ2 =9.5 5 ,P =0 .0 0 8)。协同存在AGT TT型时 ,ACE(I D)基因多态性与EH LVH有关 (χ2 =6 .2 2 ,P =0 .0 4 4 ) ,且D等位基因在EH LVH明显增高 (χ2 =6 .91,P =0 .0 0 9) ,该类EH患者发生LVH的相对危险度增高 (OR :2 .5 0 ,95 %CI:1.2 5~ 5 .0 0 )。结论 ACE(I D)基因多态性D等位基因可能是LVH的独立危险因子。ACE基因多态性与AGT基因多态性之间的协同效应表明 ,同时携带AGT TT型时 ,具有ACE(I D)基因多态性D等位基因的EH患者更易发生LVH。  相似文献   

16.
BACKGROUND AND AIMS: A single-nucleotide variant of the angiotensinogen gene (AGT 235T) has been associated with essential hypertension and increased plasma levels of angiotensinogen. This variant may also serve as a genetic marker for the increased blood pressure response to dietary salt intake, but the relationship between AGT genotype and salt sensitivity has not been studied until now. We therefore examined the relationship between the AGT 235T genotype and the blood pressure response to short-term dietary salt restriction in young normotensive men. SUBJECTS AND METHODS: A total of 187 young normotensive men were characterized for family history of hypertension, salt sensitivity, plasma parameters of the renin-angiotensin system under high- and low-salt diets, and the AGT 235T genotype. RESULTS: While the T allele was significantly associated with a positive family history of hypertension (chi2 = 7.0; P< 0.03) and higher plasma angiotensinogen levels (P< 0.015) and renin activity (P < 0.037), blood pressure under both diets was not significantly affected by the AGT genotype. When the subjects were classified into salt-resistant and salt-sensitive groups, genotypic distribution was nearly identical between both groups (frequency of T allele: 0.45 versus 0.46). CONCLUSION: Our findings demonstrate that the AGT 235T allele is significantly associated with a positive family history of hypertension, but is not an important determinant of the blood pressure response to dietary salt intake in young normotensive subjects. It is therefore unlikely that the AGT 235T genotype can serve as an early genetic marker of salt sensitivity.  相似文献   

17.
BACKGROUND AND AIM OF THE STUDY: It has been reported that patients with mitral valve prolapse syndrome (MVPS) also have a disorder in autonomic or neuroendocrine function which can cause many related symptoms. Although a potential role of the reninangiotensin system in the pathogenesis of MVPS has been addressed, the role of the angiotensinogen (AGT) genetic variant in MVPS has not been studied. Thus, a case-controlled study was performed to investigate the possible relationship between AGT gene polymorphisms and MVPS. METHODS: A total of 100 patients with MVP diagnosed by echocardiography and 100 age- and sex-matched normal control subjects was studied. AGT gene M235T and T174M polymorphisms were identified by polymerase chain reaction-based restriction analysis. RESULTS: There was a significant difference in the distribution of AGT gene M235T genotypes (p <0.001) and allelic frequencies (p <0.001) between MVPS cases and controls. An Odds Ratio (OR) for risk of MVPS associated with M235T TT genotype was 8.55 (95% CI 4.51-16.18). An OR for risk of MVPS associated with the T allele at the M235T locus of the AGT gene was 3.27 (95% CI 2.05-5.22). The T174M polymorphism of AGT gene showed no association with MVPS (p = 0.94). CONCLUSION: These findings suggest that the M235T polymorphism of the AGT gene is associated with MVPS in the Chinese population of Taiwan. The association of the TT genotype with MVPS is more noteworthy than an overall increase in the frequency of the T allele at the M235T locus.  相似文献   

18.
BACKGROUND: Malignant hypertension can be considered an extreme phenotype of renin-mediated hypertension. Therefore, we compared the allelic frequencies of the angiotensinogen (AGT) M235T, angiotensin-converting enzyme insertion/deletion (ACE I/D) and angiotensin II-type I receptor (AT1R) A1166C polymorphisms in malignant hypertensive patients with hypertensive and normotensive controls. METHODS: A total of 101 consecutive patients between 1995 and 2005 admitted to a large university hospital fulfilled the criteria for malignant hypertension. Seventy-five patients (74%) were compared with 150 hypertensive and 150 normotensive controls, randomly selected from a population study and individually matched on age, sex and ethnicity. RESULTS: The odds of malignant hypertension in white subjects with the TT genotype of the AGT M235T polymorphism was 14.3 (5.5-37) compared to hypertensive controls, and 9.4 (3.8-23.2) compared to normotensive controls. Adjustment for age, sex, smoking and antihypertensive therapy did not affect this association. The association of AGT M235T with malignant hypertension was not significant in blacks. In patients with malignant hypertension, the TT genotype was associated with more severe renal dysfunction and microangiopathic haemolysis. No differences were found in allele frequencies of the ACE I/D or the AT1R A1166C polymorphisms between study groups. CONCLUSIONS: The TT genotype of AGT M235T is associated with malignant hypertension in whites, carriers having an odds of approximately 10 to 1 compared to hypertensive and normotensive controls. These observations may provide a better understanding of the pathophysiology of malignant hypertension and offer possibilities for identifying patients at risk. Larger association or linkage studies are needed for a more detailed risk assessment.  相似文献   

19.
目的:探讨血管紧张素原基因M235T突变与家族性原发性高血压(EH)的关系。  方法:应用脱氧核糖核酸(DNA)杂交和测序检定方法,对一个典型原发性高血压大家系100名成员[分直系亲属高血压组(n= 45)、直系亲属正常血压组(n= 38)及非直系亲属正常血压组(n= 17)]和正常血压对照家系直系亲属21 名(为正常对照组)成员按< 35岁和≥35岁2个年龄层的M235T突变进行分析。  结果:比较4组在< 35 岁和≥35 岁2个年龄层的M235T分布。表明各年龄层中,4组间M235T基因型及基因频率分布未见显著不同。  结论:血管紧张素原基因M235T突变与该家族性原发性高血压没有显著关联;M235T突变可能不是该家族性原发性高血压的遗传易感因素。  相似文献   

20.
BACKGROUND: The relations of the angiotensinogen (AGT) T174M and M235T gene polymorphisms to the risk of coronary heart disease (CHD) have been investigated in only a few studies with conflicting results. RESULTS: Therefore, we analysed the relationship of the AGT gene polymorphisms to the presence and extent of CHD in 2250 male Caucasians whose coronary anatomy was defined by means of coronary angiography. The relative frequencies of the T and M alleles of the T174M and of the M235T gene variation did not significantly differ between patients without or with single-, double- or triple-vessel disease and between subjects without or with myocardial infarction (MI). In contrast the mean CHD score--defined by Gensini--was higher within MM homozygotes of the T174M gene variation than within TT genotypes; TM subjects had intermediate values. In M235T genotypes, mean CHD scores were similar in the total sample and in older individuals (> or = 62 years), whereas in younger individuals (< 62 years) a higher CHD score was found within AGT 235 T allele carriers than within MM homozygotes. In younger individuals with high apoAI plasma levels, the mean CHD score was clearly higher within TT homozygotes of the M235T gene variation than within MM genotypes; MT subjects had intermediate values. An interaction between both angiotensinogen gene polymorphisms on the extent of CHD or on the risk of non-fatal MI were not observed when the M allele of AGT T174M was combined either with the T allele or the TT genotype of M235T. CONCLUSIONS: The present study strengthens the hypothesis of an association of both angiotensinogen gene polymorphisms with the extent of coronary heart disease.  相似文献   

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