ACE基因I/D和AT1R基因A1166C多态性与氢氯噻嗪降压疗效的相关性研究

目的 探讨血管紧张素转换酶(ACE)基因I/D与血管紧张素Ⅱ-1型受体(AT1R)基因A1166C多态性与氢氯噻嗪(HCTZ)降压疗效的关系.方法 原发性高血压患者服用HCTZ 6周后,按不同ACE基因型和AT1R基因型分组,比较不同基因型组合患者的血压下降值.结果 ACE基因DD、ID、II基因型患者收缩压均下降,DD基因型患者收缩压下降值显著大于ID、II型患者(P＜0.05);AT1R基因AC(CC)和AA基因型患者收缩压下降值组间比较无显著差异(P＞0.05);DD AC(CC)基因型组合患者收缩压亦下降,与其他基因型组合患者比较无显著差异(P＞0.05).多因素分析结果表明,治疗前醛固酮浓度和DD基因型是影响患者收缩压下降的主要因素.结论 ACE基因的DD基因型与HCTZ的降压疗效相关;AT1R基因AC(CC)、DD AC(CC)型组合患者对HCTZ的降压反应可能优于其他基因型组合患者.     

血管紧张素转换酶基因型与氢氯噻嗪降压疗效的相关性研究

目的　探讨高血压病患者血管紧张素转换酶 (ACE)基因不同基因型与氢氯噻嗪降压疗效的关系。方法　 5 18例高血压病患者同时服用氢氯噻嗪 12 5mg ,每日 1次 ,共 6周。资料完整的 5 0 4例患者按II、ID、DD三种基因型分组 ,比较不同基因型间的降压疗效。结果　II、ID、DD基因型患者收缩压下降值分别为 5 7mmHg(1mmHg =0 133kPa)、5 1mmHg、10 4mmHg ,DD基因型患者收缩压下降值大II、ID两型患者 ,差异具有统计学意义 (P <0 0 5 ) ;三组间舒张压下降值、平均动脉压下降值差异无统计学意义 (P >0 0 5 ) ;多元线性回归结果表明DD基因型、治疗前醛固酮水平、血钠水平是影响收缩压下降值的主要因素。结论　不同ACE基因型患者对氢氯噻嗪的反应存在差异 ,DD基因型患者收缩压下降最明显。     

海南黎族血管紧张素转换酶基因多态性与高血压并动脉硬化的相关性研究

目的 探讨海南黎族人群血管紧张素转换酶(ACE)基因多态性与高血压并动脉硬化的相关性.方法 采用聚合酶链反应(PCR)检测260例海南黎族动脉硬化患者组及276例黎族健康人对照组的ACE基因插入或缺失(I/D)多态性,观察DD、DI、Ⅱ基因型频率及等位基因频率.用高分辨超声技术分别检测DD、DI、Ⅱ 3个亚组的平均颈动脉内-中膜厚度(MIMT). 结果 (1)动脉硬化组DD、DI、Ⅱ基因型频率为15.0%、37.3%、47.7 ;D及Ⅰ等位基因频率分别为33.7%及66.3%.对照组DD、DI、Ⅱ基因型频率17.8%、40.6%、41.7%,D及Ⅰ等位基因频率分别为38.0%及62.0%.两组间DD、DI、Ⅱ基因型频率及D、Ⅰ等位基因频率差异无统计学意义(P>0.05).(2)动脉硬化组在年龄、总胆固醇(TC)、三酰甘油(TG)、载脂蛋白A(apoA)、载脂蛋白B(apoB)、收缩压、舒张压显著高于对照组(P<0.05),而高密度脂蛋白胆固醇(HDL-C)显著低于对照组(P<0.05);Logistic回归分析结果 显示,TG(OR=2.14)、apoA(OR=360.39)、收缩压(OR=1.21)、舒张压(OR=1.08)、ACE DD基因型(OR=0.30)与高血压并动脉硬化相关(P<0.05).ACE DD型亚组的MIMT比DI和Ⅱ型亚组显著增高(P<0.05). 结论 ACE DD基因型增加了颈动脉硬化易感性,是海南黎族高血压并动脉硬化患者的危险因素,可作为动脉粥样硬化的一个早期预测因子.     

血管紧张素转换酶和α-Adducin基因多态性与氢氯噻嗪降压疗效

目的研究血管紧张素转换酶(ACE)基因I/D多态性和α-adducin基因G614T多态性与氢氯噻嗪降压疗效的关系.方法829例原发性高血压患者同时服用氢氯噻嗪12.5mg,1次/d,6周后资料完整的754例患者按不同ACE基因型和α-adducin基因型分组,比较不同基因型组和组合基因型组血压下降值.结果服用氢氯噻嗪6周后,DD基因型患者收缩压下降值大于II、ID型患者,差异有统计学意义(P＜0.05).TT基因型患者收缩压下降值大于GG、GT型患者,差异有统计学意义(P＜0.01);TT、GT基因型患者舒张压下降值大于GG基因型患者,差异有统计学意义(P＜0.01);多因素分析结果表明DD基因型、TT基因型、DD+TT组合基因型、治疗前醛固酮(Ald)水平是影响患者收缩压下降的主要因素.结论ACE基因I/D多态性、α-adducin基因G614T多态性均与氢氯噻嗪的降压疗效相关;DD+TT组合基因型对HCTZ的降压反应可能优于其他组合基因型.     

氨氯地平对老年收缩期高血压患者大动脉内皮功能和粥样硬化的影响

目的　评价氨氯地平对老年收缩期高血压 (EISH)患者大动脉内皮功能和粥样硬化的影响。方法　选择老年收缩期高血压患者 2 5例 ,应用高分辨超声技术检测EISH患者氨氯地平治疗 12周前后的肱动脉内皮依赖性舒张功能(FMD) ,颈动脉平均内中膜厚度 (MIMT)及颈动脉斑块的Crouse积分 ,并观察治疗前后收缩压和脉压的变化。结果 　EISH患者治疗 12周后收缩压、脉压和MIMT比治疗前明显下降 (P <0 .0 5或 <0 .0 1) ,FMD明显改善 (P <0 .0 1)。结论　氨氯地平除能有效降低EISH患者的血压外 ,还能改善大动脉内皮功能     

血管紧张素转换酶和α-Adducin基因多态性与氢氯噻嗪降压疗效

目的 研究血管紧张素转换酶(ACE)基因I／D多态性和α-adducin基因G614T多态性与氢氯噻嗪降压疗效的关系。方法 829例原发性高血压患者同时服用氢氯噻嗪12.5mg，1次／d，6周后资料完整的754例患者按不同ACE基因型和α-adducin基因型分组，比较不同基因型组和组合基因型组血压下降值。结果 服用氢氯噻嗪6周后，DD基因型患者收缩压下降值大于II、ID型患者，差异有统计学意义(P＜0.05)。TT基因型患者收缩压下降值大于GG、GT型患者，差异有统计学意义(P＜0.01)；TT、GT基因型患者舒张压下降值大于GG基因型患者，差异有统计学意义(P＜0.01)；多因素分析结果表明：DD基因型、TT基因型、DD TT组合基因型、治疗前醛固酮(Ald)水平是影响患者收缩压下降的主要因素。结论 ACE基因I／D多态性、α-adducin基因G614T多态性均与氢氯噻嗪的降压疗效相关；DD TT组合基因型对HCTZ的降压反应可能优于其他组合基因型。     

血管紧张素转换酶基因与冠状动脉粥样硬化关系的研究

目的　探讨血管紧张素转换酶 (ACE)基因多态性与冠状动脉粥样硬化的关系。方法　 14 6例冠心病(CAD)患者按ACE基因型分为缺失型纯合子 (DD)、杂合子 (ID)及插入型纯合子 (II) 3组 ;Bogaty标准评价冠状动脉造影结果 ;马尿酸微量比色法测量血清ACE水平。结果　⑴Bogaty各指标评价结果与左室射血分数 (LVEF)及左室舒张末压 (LVEDP)明显相关。⑵DD型CAD患者冠脉病变较ID及II型严重。⑶DD型CAD患者血清ACE水平高于ID及II型。结论　⑴ACE基因多态性与CAD患者冠状动脉病变有关。⑵血清ACE水平可能为二者相关的机制。⑶Bogaty标准能全面准确地反映CAD患者冠状动脉病变特征及左室功能下降程度。     

血管紧张素转换酶和醛固酮合成酶基因多态性与氢氯噻嗪降压疗效的关系

目的研究血管紧张素转换酶(ACE)基因I/D多态性和醛固酮合成酶(CYP11B2)基因-344T/C多态性与氢氯噻嗪降压疗效的关系。方法829例高血压病(EH)患者同时服用氢氯噻嗪12·5mg(1次/d),6周后资料完整的785例患者按不同ACE基因型和CYP11B2基因型分组,比较不同基因型和不同基因型组合间血压下降值有无差别。结果服用氢氯噻嗪6周后,ACE基因II、ID、DD型患者收缩压分别下降(5·1±14·8)mmHg(1mmHg=0·133kPa)、(4·8±16·3)mmHg和(9·4±15·7)mmHg,DD型患者下降值大于II、ID型患者,组间比较差异有统计学意义(P<0·00);CYP11B2基因TT、TC、CC型患者收缩压下降值分别为(5·8±16·2)mmHg、(5·5±14·9)mmHg和(7·6±16·1)mmHg,组间比较差异无统计学意义。DD+CC基因型患者收缩压下降值为(10·6±12·3)mmHg,高于其他基因型组合患者,但差异无统计学意义(P>0·05)。多因素分析结果表明DD基因型和治疗前醛固酮浓度是影响患者坐位收缩压下降的主要因素。结论ACE基因的DD型与氢氯噻嗪的降压疗效相关,CYP11B2基因CC型、DD+CC型患者对氢氯噻嗪的降压反应可能优于其他基因组合患者。     

ACE基因导向治疗对高血压及颈动脉内膜中层厚度的影响

目的探讨经血管紧张素转化酶(ACE)基因导向治疗后对高血压患者颈动脉内膜中层厚度(IMT)变化的影响。方法随机选择原发性高血压患者80例,对照组、基因导向治疗A组(Ⅱ型)、B组(ID型)和C组(DD型)各20例。基因导向治疗A组选用依那普利15 mg,基因导向治疗B组选用依那普利10 mg,基因导向治疗C组选用依那普利5 mg,对照组选用依那普利10 mg,均1次/d口服进行治疗。所有患者分别于入院当天、治疗3、6、9个月跟踪回访行颈动脉彩超检查,记录颈动脉IMT变化情况,同时监测血压变化。分别比较四组患者不同时间点颈动脉内膜厚度变化及血压变化。结果 3个基因导向治疗组与对照组相比,IMT、IMI/内径比率(diameter)、收缩压(SBP)及舒张压(DBP)随时间变化逐渐降低(P<0.05),且基因导向治疗C组下降幅度均大于基因导向治疗B组,基因导向治疗B组下降幅度均大于基因导向治疗A组。结论原发性高血压患者根据ACE基因多态性分型进行基因导向治疗(主要是DD型和ID型),可有效降低原发性高血压患者颈动脉IMT,有效控制血压。     

亚甲基四氢叶酸还原酶C677T位点基因多态性对采用叶酸联合维生素B_(12)治疗的老年H型高血压患者的影响研究

目的探讨亚甲基四氢叶酸还原酶(MTHFR)C677T位点基因多态性对采用叶酸联合维生素B_(12)治疗的老年H型高血压患者的影响。方法选取2015年9月—2017年9月莱芜市人民医院收治的老年H型高血压患者146例,均在常规降压治疗基础上采用叶酸联合维生素B_(12)连续治疗4个月。采用聚合酶链反应(PCR)-芯片杂交法检测MTHFR C677T位点基因多态性,比较不同基因型患者高血压分级,治疗前后血浆同型半胱氨酸(Hcy)水平、颈动脉粥样硬化斑块积分及不稳定斑块检出率。结果 146例患者中CC基因型26例(占17.8%),CT基因型46例(占31.5%),TT基因型74例(占50.7%)。不同基因型患者高血压分级比较,差异无统计学意义(P0.05)。治疗前、后TT基因型患者血浆Hcy水平高于CC基因型、CT基因型(P0.05)。治疗后CC基因型、CT基因型患者血浆Hcy水平低于治疗前(P0.05)。治疗前、后TT基因型患者颈动脉粥样硬化斑块积分高于CC基因型、CT基因型,CT基因型患者颈动脉粥样硬化斑块积分高于CC基因型(P0.05)。治疗后CC基因型、CT基因型患者颈动脉粥样硬化斑块积分低于治疗前(P0.05)。治疗前、后不同基因型患者颈动脉不稳定斑块检出率比较,差异无统计学意义(P0.05)。结论叶酸联合维生素B_(12)降低老年H型高血压患者血浆Hcy水平、颈动脉粥样硬化斑块积分效果与MTHFR C677T位点基因多态性有关,其中TT基因型患者的降低效果不如CC基因型、CT基因型,临床应当考虑遗传因素和基因多态性。     

性别因素对原发性高血压候选基因研究的影响作用

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。     

白大衣高血压血管紧张素转换酶基因多态性分析

目的：研究白大衣高血压与血管紧张素转换酶（angiotensin converting enzyme，ACE）基因I／D多态性的关系。方法：应用多聚酶链式反应（PCR）方法对白大衣高血压，高血压病Ⅰ级患者和正常血压者各30例进行ACE I／D基因型检测，并分析比较。结果：白大衣高血压和高血压病Ⅰ级组Ⅱ基因型低于正常组（P〈0．01），白大衣高血压和高血压病Ⅰ级组DD基因型高于正常组（P〈0．01），白大衣高血压ID基因型显著高于高血压病Ⅰ级组和正常组（P〈0．01）。高血压病Ⅰ级组ID基因型低于正常组（P〈0．01）。结论：白大衣高血压与ACE基因多态性有关，ID基因型者易患白大衣高血压。     

原发性高血压病人群ACE基因的多态性与血管损害相关性的研究

目的探讨血管紧张素转化酶（ＡＣＥ）基因插入／缺失（Ｉ／Ｄ）多态性与中国原发性高血压（ＥＨ）人群血管并发症之间的关系。方法应用ＰＣＲ技术扩增位于ＡＣＥ基因第１６内含子的一基因片段,共检测ＥＨ患者２０４例和正常对照９６例。结果ＥＨ组ＤＤ、ＤＩ、Ｉ型基因的分布频率与对照组无显著性差异,但三期ＥＨ亚组ＤＤ型基因及Ｄ等位基因的分布频率高于正常对照组（Ｐ＜０．０１）。血浆ＡＣＥ活性与基因类型的关系为ＤＤ＞ＤＩ＞Ｉ。结论中国原发性高血压人群ＡＣＥ基因１６内含子插入／缺失多态性与其血管并发症密切相关。     

Angiotensin-converting enzyme gene polymorphism and its association with essential hypertension in a Tibetan population.

There is strong evidence to support the idea that the renin-angiotensin system (RAS) plays an important role in the pathogenesis of essential hypertension (EH) and its complications. However, existing data about the association of angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism with blood pressure is conflicting, mainly due to racial differences and environmental exposure status. We therefore conducted a case control study to observe the relationship between ACE I/D polymorphism and EH in a Tibetan population who live in relatively isolated areas and are genetically homogeneous. The study was conducted at stable residential communities in the urban district of Lhasa, the capital of the Tibet autonomous region, China, and 106 unrelated EH patients and 135 normotensIve subjects were recruited. PCR, PCR/RFLP and PCR-SSCP were carried out to study the association between RAS genes and EH. Frequencies for the DD, ID and II genotypes were 27, 47 and 29 in hypertensive subjects, and 15, 60 and 48 in normotensive subjects, respectively. Derived allele frequencies for the I and D alleles were 0.51 and 0.49 in hypertensive subjects and 0.64 and 0.36 in normotensive subjects. There were significant differences in genotype distribution and derived allele frequency between these two groups. The genotype and allele frequencies of the ACE gene differed significantly between hypertensive and normotensive females (p>0.05), but there were no differences in males. In females, the DBP and MAP level were significantly higher for the DD than for the ID and II genotype, and SBP was significantly higher for the DD than for the II genotype. But in males, there were no significant differences in blood pressure among ACE genotypes. The results showed a significant association between the D allele of the ACE gene and hypertension in Tibetan women but not in Tibetan men.     

冠心病与血管紧张素转换酶和内皮型一氧化氮合酶基因多态性及交互作用的临床研究

目的联合对冠心病患者血管紧张素转换酶（ACE）基因多态性和内皮型一氧化氮合酶（eNOS）基因G894T多态性进行分析,探讨基因多态性与冠心病的关系和交互作用及遗传学机制在冠心病发病及预后中的临床意义。方法应用聚合酶链反应-限制性片段长度多态性（PCR—RFLP）分析技术检测236例冠心病患者及190例正常人ACE和eNOS两种基因多态性。同时测定血脂、血糖、体重指数（BMI）、左室射血分数（LVEF）和血压。结果冠心病组ACE基因DD型频率[36％（86／236）]显著高于对照组[19％（36／190）,P〈0．01],Ⅱ型频率[27％（64／236）]显著低于对照组[49％（93／190）,P〈0．05]。冠心病组DD型甘油三酯（TG）[（2．2±1．7）mmol／L]显著高于Ⅱ型TG[（1．6±0．8）mmol／L和ID型TG[（1．7±0．9）mmol／L,均P〈0．05],DD型高密度脂蛋白胆固醇[HDL—C（1．2±0．4）mmol／L]显著低于Ⅱ型HDL—C[（1．3±0．3）mmol／L,P〈0．05],DD型血糖[（6．2±1．7）mmol／L]和BMI[（25．7±2．8）kg／m^2]显著高于ID型[血糖：（5．6±1．3）mmol／L,BMI：（24．8±3．1）kg／m^2。,P〈0．05],DD型LVEF（56％±14％）显著低于Ⅱ型LVEF（62％±15％）和ID型LVEF（61％±14％）,均P〈0．05。收缩压、舒张压、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL—C）、糖尿病组与非糖尿病组、急性冠状动脉综合征组与非急性冠状动脉综合征组、单支病变组与多支病变组在ACE和eNOS基因不同基因型之间差异均无统计学意义。冠心病组eNOS基因GT型频率[28％（67／236）]显著高于对照组[17％（32／190）,P〈0．01],GG型频率与对照组比较,差异无统计学意义。TG、HDL—C、血糖、BMI和LVEF在eNOS基因不同基因型之间差异均无统计学意义（均P〉0．05）。携带DD型患冠心病的概率是携带Ⅱ型的1．74倍（P〈0．01）,携带GT型患冠心病的概率是携带GG型的1．73倍（P〈0．05）。两种基因对患冠心病的交互作用显示为如同时携带Ⅱ型和GG型,患冠心病的概率是37．9％,而同时携带DD型和GT型患冠心病的概率是77．8％。结论ACE基因多态性和eNOS基因多态性与冠心病及某些危险因素显著相关,同时携带DD型和GT型两种易患基因型时,患冠心病的概率明显增加,具有显著的遗传倾向。     

Relationship between polymorphism of the angiotensin-converting enzyme gene and the response to angiotensin-converting enzyme inhibition in hypertensive patients.

The aim of this study was to investigate the relationship between polymorphism of the anglotensin-converting enzyme (ACE) gene and the blood pressure response to ACE inhibition in a hypertensive cohort. Imidapril (5-10 mg/day) or benazepril (10-20 mg/day) was administered for 6 weeks to 517 essential hypertensives. ACE gene polymorphism was examined by the polymerase chain reaction (PCR) method and the patients were classified as having the 190-bp deletion homozygous (DD) genotype, the 490-bp insertion homozygous (II) genotype, or the 490-bp insertion, 190-bp deletion heterozygous (ID) genotype. The achieved change in systolic and diastolic blood pressure (SBP and DBP) was analyzed for association with genotypes at the ACE gene locus. The DD genotype was observed in 132 patients (25.5%), the ID genotype in 255 patients (49.3%), and the II genotype in 130 patients (25.2%). The SBP reductions in the patients with the DD genotype, II genotype, and ID genotype were -14.5 +/- 12.7 mmHg, -14.3 +/- 13.1 mmHg and -14.0 +/- 12.2 mmHg, respectively (p = 0.94). The DBP reductions in the patients with the DD genotype, II genotype, and ID genotype were -8.7 +/- 7.4 mmHg, -8.7 +/- 7.7 mmHg and -8.5 +/- 6.7 mmHg, respectively (p = 0.96). There was no significant association between the ACE gene polymorphisms and the response to ACE inhibition. These results suggest that ACE genotype does not predict the blood pressure-lowering response to antihypertensive treatment with ACE inhibition.     

Angiotensin-converting enzyme gene polymorphism influences degree of left ventricular hypertrophy and its regression in patients undergoing operation for aortic stenosis.

Insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been associated with increased left ventricular hypertrophy (LVH) in patients with cardiomyopathy and congestive heart failure. Patients with aortic stenosis (AS) have varying degrees of LVH at a given valve area. The aim of this study was to examine the relation between ACE gene polymorphism and the degree of LVH in patients undergoing operation for AS. Eighty-two patients who underwent operation for AS with a stentless valve were followed prospectively with echocardiographic assessments of left ventricular mass index (LVMI). ACE gene polymorphism was determined by polymerase chain reaction. The genotype (DD, ID, and II) frequency was the same as in healthy controls. The pressure difference across the aortic valve did not differ between genotypes. Patients with the DD genotype of the ACE gene had a higher LVMI (197 +/- 47 g/m2) preoperatively than those with ID (175 +/- 41 g/m2) or II (155 +/- 43 g/m2) genotypes (p = 0.01). LVMI decreased significantly in DD (p <0.001) and ID (p <0.001) genotypes but not in the II genotype during follow-up (mean 15 months). There was a significant difference in regression of LVMI over time between genotypes (p = 0.0056), with no significant difference between genotypes at follow-up. The DD genotype of the ACE gene is associated with increased preoperative LVH in patients treated surgically for AS. The DD genotype appears to be an important factor which increases hypertrophic myocardial reactivity to pressure overload.     

血管紧张素转化酶多态性与北京降压0号长期降压效果的关系

目的:探讨不同血管紧张素转化酶(ACE)基因插入/缺失(I/D)多态性的基因型的原发性高血压(EH)患者对北京降压0号治疗的长期反应性。方法:根据ACE I/D基因多态性,将EH患者分为II组(16例),ID组(11例)及DD组(15例),共42例。使用北京降压0号1片/d,共1年,观察降压疗效。结果:II组显效10例,有效5例,总有效率93.8%;ID组显效5例,有效4例,总有效率81.8%;DD组显效11例,有效2例,总有效率86.7%,控制率分别为75.0%、72.7%、60.0%,各组疗效差异无统计学意义(P>0.05),3组平均血压下降值比较,舒张压下降值II组高于ID组(P<0.05),其余均差异无统计学意义。结论:ACE I/D基因多态性对北京降压0号治疗EH的长期效果无影响。     

Predicting Response to Chronic Antihypertensive Treatment with Fosinopril: The Role of Angiotensin-Converting Enzyme Gene Polymorphism

Insertion (I)/deletion (D) polymorphism of the ACE gene has been reported to be involved in various cardiovascular diseases. We investigated prospectively whether the response to the ACE inhibitor fosinopril varied according to the ACE genotype in previously untreated Greek hypertensive patients. After a 4-week observation period, fosinopril was administered at a dose of 20 mg daily and blood pressure was measured weekly for 6 months. The study population consisted of 104 hypertensive patients (46 male, 58 female). There were no differences in age, gender, body mass index, and pretreatment blood pressure levels among patients with the DD, ID, and II genotypes (n = 42, 30, 32, respectively). The reduction in systolic blood pressure was significantly greater in patients carrying the DD compared to II or ID genotypes (5.6 ± 3.1 vs. 3.1 ± 1.1 or 3.6 ± 2.2, respectively; ANOVA, p < 0.05). The reduction in diastolic blood pressure was also significantly greater in DD hypertensives compared with II or ID (8.9 ± 6 vs. 5.5 ± 3.4 or 5.8 ± 4, respectively; ANOVA, p < 0.05). The age and BMI were not correlated with the changes in SBP or DBP that were observed after fosinopril administration. In conclusion, the ACE gene genotype was shown to influence the response to fosinopril in hypertensive patients.