血管紧张素转换酶基因多态性与原发性高血压血栓前状态的关系

目的　探讨血管紧张素转换酶 (ACE)基因I/D多态性与原发性高血压 (EH)及高血压血栓前状态 (PTS)的关系。方法　PCR检测 6 1例原发性高血压病人和正常对照组 2 8例的ACE基因I/D多态性 ;发色底物法测t PA、PAI 1活性 ,酶联免疫吸附双抗夹心法 (ELISA)测vWF含量。结果　高血压组DD基因型频率显著高于对照组 (P <0 0 5 ) ,但D等位基因频率分布在高血压组和正常组之间差异无显著意义 (P >0 0 5 )。高血压组t PA活性降低 ,PAI 1活性、vWF含量升高 (P均 <0 0 0 1)。高血压组DD型t P活性明显低于ID、II型 (P <0 0 0 1) ,而ID、II型之间差异无显著意义 (P >0 0 5 ) ,DD型PAI 1活性明显高于ID、II型(P <0 0 0 1) ,而ID、II型之间差异无显著意义 (P >0 0 5 ) ,vWF在DD、ID、II型三者之间差异无显著意义 (P>0 0 5 )。结论　DD型是原发性高血压发病的危险因素。原发性高血压存在血栓前状态。t PA、PAI 1的变化与血管紧张素转换酶基因I/D多态性有关 ,DD基因型可引起血栓前状态。     

ACE基因多态性与原发性高血压及左心室肥厚的关系

目的 :探讨中国汉族人群血管紧张素转化酶基因插入/缺失 (I/D)多态性与原发性高血压及左心室肥厚的关系。方法 :应用PCR技术测定108例健康对照者和146例原发性高血压患者的ACE基因型 ,并进行心脏彩超检查 ,计算左室质量指数 ,然后进行统计学分析。结果 :(1)108例健康对照者中DD基因型频率17%、ID型37%、Ⅱ型46% ,原发性高血压组DD型21%、ID型39%、Ⅱ型40% ,两组比较 (P>0 05) ,ACE基因多态性在正常对照组与高血压组中差异无显著性。(2)75例高血压伴左室肥厚患者中 ,DD基因型频率29%、ID型35%、Ⅱ型36% ,而71例高血压不伴左室肥厚患者中 ,DD型13%、ID型43 5%、Ⅱ型43 5% ,两组比较P<0 05,DD基因型频率在高血压伴左室肥厚患者中高于高血压不伴左室肥厚患者。结论 :ACE的3种基因型与原发性高血压发病无关 ,但与高血压左心室肥厚的发生有关 ,DD基因型的高血压患者易出现左心室肥厚     

复发性脑梗死与血管紧张素转换酶基因多态性的关系

目的：评价血管紧张素转换酶（ACE）基因多态性与脑梗死发生和复发及其危险因素的关系。方法：测定复发及首发性脑梗死患者各60例，提取DNA做ACE基因多态性检测。结果：DD基因型频率和D等位基因频率在复发性脑梗死患者中明显增加（均P＜0．01），伴有高血压脑梗死患者DD基因型频率明显高于无高血压患者（P＜0．05），且伴有脑血管病（CVD）家族史者DI基因型明显高于无家族史者（P＜0．01），结论：ACE基因多态性可能和脑梗死的复发有关，在高血压人群和有脑血管病家族史的人群中进行ACE基因调查，可及早发现脑梗死发生和复发的高危人群，对脑梗死的防治意义重大。     

ACE基因多态性和高血压合并脑出血的关系探讨

目的探讨血管紧张素转换酶(ACE)基因多态性和高血压合并脑出血的关系。方法选取2019年7月至2020年7月广东省潮州市人民医院收治的35例高血压合并脑出血患者和35例健康体检者作为研究对象。检测两组患者ACE基因插入/缺失(I/D)位点多态性并统计两组各项资料行单因素分析,将单因素分析具备统计学意义的变量进一步行多因素Logistics回归分析ACE基因多态性和高血压合并脑出血间的相关性。结果单因素分析结果显示,两组年龄 65岁、吸烟史、体重指数(BMI)组间差异有统计学意义(P 0.05),两组ACE基因多态频率差异无统计学意义(P 0.05);但高血压合并脑出血患者DD基因型频率和D等位基因频率高于健康体检者(P 0.05);多因素Logistics回归分析显示,携带ACE基因D等位基因BMI、年龄 65岁、吸烟史是高血压合并脑出血的独立危险因素(P 0.05)。结论 ACE基因多态性携带的D等位基因与高血压合并脑出血间存在明显相关性,可能是高血压合并脑出血的危险因素。     

天津市支气管哮喘病人血管紧张素转移酶基因多态性研究

目的　探讨血管紧张素转移酶 (ACE)基因插入 (insertion,I)与缺失 (deletion,D)多态性与支气管哮喘易感性的关系。方法　采用聚合酶链反应 (PCR)方法检测 18例哮喘患者 ,15名正常健康对照者的 ACE基因型。结果　哮喘组 ACE基因中 DD基因型频率和 D等位基因频率分别为 6 1%和 72 % ,而正常对照组为 2 0 %和37% ,两组比较差异有统计学意义 (P<0 .0 5 )。结论　提示 ACE基因 DD等位基因型与哮喘的遗传易感性相关 ,可能是哮喘的危险因素之一。     

血管紧张素转换酶基因多态性与重度子痫前期及肾功能损害的关系

目的 探讨血管紧张素转换酶(ACE)基因第16内含子插入/缺失(I/D)多态性与重度子痫前期和子病前期肾功能损害的关系.方法 采用聚合酶链反应(PCR)技术检测120例子痫前期(其中轻度67例,重度53例)和60例正常孕妇ACE基因I/D多态性.结果 重度子痫前期组分别与正常孕妇组和轻度子痫前期组比较,ACE基因型分布和等位基因频率均有显著差异(P＜0.01);子痫前期肾功能损害组与无肾功能损害组比较,ACE基因型分布有显著差异(P＜0.05).结论 ACE基因I/D多态性与子痫前期病情相关;ACE基因I/D多态性与子痫前期肾功能损害相关,DD基因型可能是子痫前期肾功能损害的危险因素.     

ACE多态性与原发性高血压合并冠心病相关性研究

目的评估血管紧张素转换酶（ACE）基因多态性与原发性高血压合并冠心病的关系。方法选择高血压组64例，冠心病组81例，原发性高血压合并冠心病组92例，健康对照组122例，采用聚合酶链反应技术检测ACE基因多态性，并比较其基因型及等位基因频率。结果高血压与冠心病组ACE基因多态性分别与对照组比较均无统计学差异，原发性高血压合并冠心病组ACE基因型频率与对照组比较有统计学差异，ACE基因多态性与原发性高血压合并冠心病相关，P〈0．001。结论ACE基因多态性可能是佛山地区原发性高血压合并冠心病的危险因素。     

ACE基因I/D多态性、血清ACE、血栓调节蛋白、体质指数对原发性高血压的影响

目的:探讨ACE基因第16内含子I/D多态性、血清ACE、血清TM、超重及其相互关系对原发性高血压的影响。方法:对从青岛市5个社区中筛检出的、未经药物系统治疗的235例原发性高血压病人及240例血压正常者进行调查,用聚合酶链反应-限制性片段长度多态性(PCR-RFLP)方法检测ACE基因I/D多态性;应用相关分析及相加模型分析I/D多态性与血清ACE、血清TM、超重的相互关系。结果:高血压组D等位基因频率(48.09%)及超重率(86.81%)高于对照组(37.08%,70.83%),(X~2=6.632,P0.05,OR=1.661;c2=18.100,p0.001,OR=2.710)。高血压组中血栓调节蛋白浓度与baPWV呈正相关(r=0.516,P0.01)。原发性高血压患者的血清ACE水平也比对照组高(P﹤0.01)。多元线性回归显示,原发性高血压、DD基因型、ID基因型与血清ACE水平有关。ACE基因I/D多态性与超重具有正交互作用。结论:ACE基因第16内含子I/D多态性、血清ACE、血清TM、超重与原发性高血压有关,I/D基因多态性与超重具有正交互作用,控制体质指数可以降低居民原发性高血压患病的危险性。     

血管紧张素转换酶基因多态性与血管紧张素转换酶抑制剂的降压作用

目的:从基因多态性研究药效的差异。方法:选择健康志愿者99 例,未治疗的原发性高血压病人40 例,用PCR 方法检测血管紧张素转换酶(ACE) 基因的插入与缺失(I/D) 多态性, 用血管紧张素转换酶抑制剂(ACEI) 卡托普利治疗高血压病人。结果:正常人与原发性高血压患者的ACE等位基因频率及基因型频率无显著差异(P>0.05) 。卡托普利降压有效病人与无效病人ACE 基因的I/D等位基因频率及基因型频率,基因缺失型纯合子(DD)或/ 和杂合子(ID) 与非缺失型(II) 也均无显著差异(P>0.05) 。结论: ACE基因的I/ D多态性与原发性高血压的发病无关, ACEI降压作用的个体差异与ACE基因的I/D多态性无关。     

山西籍汉族血管紧张素转换酶基因多态性与高血压遗传的研究

目的　研究山西籍汉族人血管紧张素转换酶 (angiotension converting enzym e,ACE)基因多态性与原发性高血压 (essential hypertension,EH)间的相互关系 ,采用三条引物法进行基因分型检测。方法　对 41个EH核心家系的 12 3例患者以及正常对照组 98名成员 ,用三条引物法进行基因分型检测。结果　 EH组 ,ACE基因型的分布频率为 :DD型 0 .10 ,ID型 0 .40 ,II型 0 .5 0 ,等位基因频率为 :D0 .30 ,I0 .70。 EH组与对照组基因型和等位基因频率差异无显著性。结论　 ACE基因 I/ D多态性与山西籍汉族人群高血压病无关联 ,三条引物法可以 1次完成 ACE基因分型     

Management of essential hypertension

Hypertension, in spite of a very high prevalence, remains undertreated. This is not due to a lack of effective therapeutic modalities. Non-pharmacological treatments can be effective in many patients. If those treatments fail to reduce blood pressure sufficiently, the physician can choose between numerous classes of antihypertensive agents. However, interpatient variability in response to these agents is high, and use of multiple agents is frequently necessary. Thus, no single class has proven to be superior for the majority of patients. This article will review the different non-pharmacological and pharmacological methods available to treat hypertension, as well as the guidelines that are available to aid in proper selection of a treatment regimen.     

Homocysteine and essential hypertension

The authors examine the available clinical and experimental data supporting the view that homocysteine, an alternative risk factor of cardiovascular disease, may play a role in the pathogenesis of essential hypertension. The mechanism of this disease has not been elucidated, but it may be related to impairment of vascular endothelial and smooth muscle cell function. Therefore, the occurrence of endothelial dysfunction could contribute to alterations of the endothelium-dependent vasomotor regulation. Elevated homocysteinemia diminishes the vasodilation by nitric oxide, increases oxidative stress, stimulates the proliferation of vascular smooth muscle cells, and alters the elastic properties of the vascular wall. Thus, homocysteine contributes to elevate the blood pressure. Also it is known that elevated plasma levels of homocysteine could lead to oxidant injury to the endothelium. The correction of elevated homocysteinemia by administration of vitamins B12 and B6 plus folic acid, could be a useful adjuvant therapy of hypertension. However, further controlled randomized trials are necessary to establish the efficacy and tolerability of these potentially therapeutic agents.     

Management of essential hypertension

Hypertension, in spite of a very high prevalence, remains undertreated. This is not due to a lack of effective therapeutic modalities. Non-pharmacological treatments can be effective in many patients. If those treatments fail to reduce blood pressure sufficiently, the physician can choose between numerous classes of antihypertensive agents. However, interpatient variability in response to these agents is high, and use of multiple agents is frequently necessary. Thus, no single class has proven to be superior for the majority of patients. This article will review the different non-pharmacological and pharmacological methods available to treat hypertension, as well as the guidelines that are available to aid in proper selection of a treatment regimen.     

Labetalol in essential hypertension

Labetalol is an orally active adrenoreceptor-blocking drug which is a competitive antagonist of both alpha- and beta-adrenoreceptor sites. Thirty patients with essential hypertension were admitted to the study. The mean of initial systolic and diastolic blood pressures of these patients was 160/101 +/- 3/1 supine and 155/104 +/- 3/1 mm Hg standing, and the mean blood pressures at the end of the 16 week trial was 142/90 +/- 4/2 supine and 131/91 +/- 3/2 mm Hg standing. The average dose of labetalol was 546 mg: eight patients received a dose of 300 mg, seven a dose of 600 mg, six a dose f 900 mg, and two a dose of 1,200 mg. The patients who needed the highest doses of labetalol had an initial lowering of their blood pressures followed by a gradual increase despite the higher doses of labetalol. There was no significant change in the mean peripheral renin activity value. Side effects were reported by 18 of the 30 patients, but only 1 patient withdrew for this reason. Two patients were considered to be treatment failures. Overall, labetalol was found to be an effective antihypertensive agent in 15 patients.     

阿罗洛尔治疗原发性高血压

目的 :观察阿罗洛尔对轻、中度高血压的治疗效果。方法 :治疗对象 6 0例 (男性 38例 ,女性 2 2例 ,年龄 55a±s11a) ,给阿罗洛尔 10mg ,qd× 6wk。结果 :服用阿罗洛尔后 1～ 3wk血压、心率逐渐下降 ,血压从治疗前的 2 2 .3/ 12 .7kPa下降到wk4的 16 .9/ 10kPa ,wk 6的 16 .4 / 9.8kPa ,心率从治疗前的 80次·min- 1下降到wk 4的 6 8次·min- 1,wk6的 6 7次·min- 1,差异均有非常显著性意义 (P <0 .0 1) ,降低血压的总有效率为 85% ,对肝、肾功能及血常规无明显影响。结论 :阿罗洛尔是一种满意的降压药。     

Bucindolol in essential hypertension

The effects of bucindolol a new nonselective beta blocker were studied after short-term dosing and for up to six months in eight patients with essential hypertension. Bucindolol 100 mg acutely lowered supine and erect systolic and diastolic pressure without orthostatic features and without increases or decreases in heart rate. Plasma noradrenaline increased, but plasma renin activity fell. Long-term dosing of 100-400 mg/day led to modest decreases in blood pressure. The duration of the hypotensive effect after multiple dosing ranged from six to ten hours. After long-term dosing there was evidence of marked nonselective beta blockade but not of alpha 1 blockade from the responses to intravenous isoprenaline and phenylephrine respectively. In six out of eight patients the plasma creatinine phosphokinase rose transiently above the normal range. The increase appeared to be of muscle origin and was associated with myalgia in one patient. Bucindolol is a nonselective beta blocker, possibly with other vasodilator properties. These do not appear to be mediated by alpha blockade.     

The causes of essential hypertension

1 Confusion between the criteria for defining and diagnosing hypertension may have misled the search for the causes of hypertension.
2 The systematic approach of molecular genetics appears to offer the best chance of explaining hypertension, but the attractions are partly offset by the large numbers required, and unproven record of the genetic techniques in finding functional mutations in complex human disorders.
3 Part of the evidence for the polygenic nature of essential hypertension derives from the variable response to a large number of different anti-hypertensive agents. Systematic investigation of this variability may provide a basis for dividing patients into genetically more homogeneous sub-groups, within which smaller numbers will be required to detect the genes responsible for the susceptibility to hypertension.
4 The proportion of hypertensive patients with affected siblings has been studied in 6000 patients from Addenbrookes Hospital and local general practices. A recurrence risk for hypertension of∼3.5 was found.
5 Approximately two-thirds of patients have no known affected siblings. The next largest group, about one third, is patients whose siblings are all hypertensive. In a small group, <10% of all patients, half the siblings are hypertensive.
6 We conclude from these surprising findings that hypertension is not a continuous, multifactorial part of the normal blood pressure distribution. They suggest that several more single-gene disorders causing hypertension will be found. The sibships where all members are hypertensive are inconsistent with the segregation of Mendelian genetics and suggest the selection of some genes linked to hypertension at the time of gamete maturation.     

Pharmacotherapy of essential hypertension.

Practical clinical aspects of the evaluation and treatment of essential hypertension are reviewed. Drug therapy discussed includes diuretics, and as adjunctive therapy, sympathoplegic agents, peripheral vasodilators and beta blockers. Also covered are treatment of less common forms of essential hypertension, other forms of antihypertensive therapy, and the use of fixed combinations of antihypertensive drugs.