螺内酯对扩张型心肌病心力衰竭患者某些体液因子的影响

目的:探讨螺内酯对扩张型心肌病心力衰竭患者血浆儿茶酚胺、肾素活性、血管紧张素Ⅱ及醛固酮的影响.方法:入选30例扩张型心肌病心力衰竭患者,随机分入螺内酯组与对照组,各15例,用螺内酯治疗前与治疗1个月后,用高效液相色谱法测定血浆去甲肾上腺素、肾上腺素,同时采用均相竞争放射免疫方法检测血浆肾素活性、血管紧张素Ⅱ与醛固酮.结果:治疗1个月后螺内酯组血浆去甲肾上腺素、肾上腺素、肾素活性、血管紧张素Ⅱ及醛固酮明显低于治疗前,也低于对照组治疗后,均有显著性差异(P＜0.05～0.01).结论:螺内酯可明显抑制扩张型心肌病心力衰竭患者的儿茶酚胺水平,降低肾素活性及醛固酮.     

螺内酯对扩张型心肌病心力衰竭患者某些体液因子的影响

目的 :探讨螺内酯对扩张型心肌病心力衰竭患者血浆儿茶酚胺、肾素活性、血管紧张素Ⅱ及醛固酮的影响。方法 :入选 2 0例扩张型心肌病心力衰竭患者 ,随机分入螺内酯组与对照组 ,各 10例 ,用螺内酯治疗前与治疗 1个月后 ,用高效液相色谱方法测定血浆去甲肾上腺素、肾上腺素 ,同时采用均相竞争放射免疫方法检测血浆肾素活性、血管紧张素 Ⅱ与醛固酮。结果 :治疗 1个月后螺内酯组血浆去甲肾上腺素、肾上腺素、肾素活性及醛固酮明显低于治疗前 ,也低于对照组。结论 :螺内酯可明显抑制扩张型心肌病心力衰竭患者的儿茶酚胺水平 ,降低肾素活性及醛固酮 ,这些改变有可能为螺内酯明显改善心力衰竭病人预后的重要机制     

螺内酯对慢性心力衰竭患者神经内分泌激素的影响

目的探讨螺内酯对慢性心力衰竭患者神经内分泌激素的影响。方法92例慢性心力衰竭患者(心功能Ⅱ~Ⅳ级),随机分为贝那普利组(对照组),贝那普利+螺内酯组(螺内酯组)。测定治疗前、治疗3个月后血浆去甲肾上腺素、肾上腺素、肾素、血管紧张素Ⅱ、醛固酮、内皮素水平的变化。结果两组治疗后血浆去甲肾上腺素、肾上腺素、内皮素水平均有明显下降(P<0.01),肾素、血管紧张素Ⅱ水平无明显变化(P>0.05)。醛固酮水平在对照组无显著变化(P>0.05),螺内酯组有显著下降(P<0.01)。结论血管紧张素转换酶抑制剂只有与螺内酯长期联合治疗才可以显著降低慢性心力衰竭患者的血浆醛固酮水平。     

苯那普利对充血性心力衰竭患者神经激素及心功能的影响

应用苯那普利对30例充血性心力衰竭患者进行为期4周的治疗，测定治疗前后血浆肾素、血管紧张素Ⅱ、醛固酮以及儿茶酚胺水平，观察心率、血压和心功能改善情况。结果显示治疗后患者血管紧张素Ⅱ、醛固酮、去甲肾上腺素、肾上腺素水平显著下降（P＜0．01），心率减慢、心功能改善，总有效率达93．3％。提示苯那普利能抑制肾素－血管紧张素－醛固酮系统，降低交感神经活性，改善充血性心力衰竭患者心功能。     

老年原发性高血压患者动态血压参数与部分体液因素的相关性研究

目的观察老年原发性高血压患者动态血压参数与血浆肾素、血管紧张素Ⅱ及醛固酮的相关性及其临床意义。方法将162例患者分为A纽82例（〉60岁）,B组80例（〈60岁）,采用放射免疫法检测162例原发性高血压患者的血浆肾素、血管紧张素Ⅱ及醛固酮水平,同时测定24h动态血压,进行相关分析。结果（1）老年高血压具有是脉压增大,波动性大,晨峰高血压现象及并发症多的特点;（2）A组血浆肾素、血管紧张素Ⅱ及醛固酮水平明显高于B组;（3）血浆肾素、血管紧张素Ⅱ及醛固酮与老年高血压的特点,特别是脉压增大、波动性大、晨峰高血压现象有关。结论老年原发性高血压患者血浆肾素和血管紧张素Ⅱ浓度升高,提示血浆肾素、血管紧张素一醛固酮系统对老年原发性高血压心血管系统有影响,导致老年原发性高血压患者血压特征性的变化,血浆肾素、血管紧张素Ⅱ和醛固酮的测定可作为老年原发性高血压患者病情监测及治疗指标之一。     

氯沙坦与依那普利治疗慢性心力衰竭对比观察

目的:探讨慢性心力衰竭时血流动力学、肾素活性、血管紧张素Ⅱ和醛固酮变化及氯沙坦对其影响.方法:慢性心力衰竭患者60例随机分为氯沙坦组和依那普利组,每组30例,疗程12周.测定治疗前、治疗1、12周血浆肾素活性、血管紧张素Ⅱ、醛固酮和治疗前、治疗12周心功能、血流动力学变化.30例健康体检者作对照组.结果:60例慢性心力衰竭患者血浆肾素活性、血管紧张素Ⅱ和醛固酮水平均较对照组升高(P＜0.01),氯沙坦组治疗后1、12周血浆肾素活性、血管紧张素Ⅱ水平较治疗前升高,以1周升高明显(P＜0.05),而12周与治疗前比较差异无显著性(P＞0.05),醛固酮水平治疗后1、12周与治疗前比较则降低,有显著差异(P＜0.01).依那普利组治疗1周、12周血浆血管紧张素Ⅱ、醛固酮水平较治疗前降低(P＜0.01),而肾素活性水平则升高,以1周升高明显(P＜0.05),而12周与治疗前比较差异无显著性(P＞0.05),治疗前后两组间比较差异无显著性(P＞0.05).氯沙坦组和依那普利组在治疗12周后,多项血流动力学指标与本组治疗前比较均有改善(P＜0.05).结论:慢性心力衰竭患者血流动力学异常、肾素-血管紧张素-醛固酮系统激活是心力衰竭病理生理特征之一,氯沙坦治疗后可获得有益的临床、血流动力学及神经激素效应,且有较好的耐受性.     

胰岛素诱发大鼠高血压机制中肾素—血管紧张素系统的作用

目的 探讨胰岛素诱发大鼠高血压机制中肾素-血管紧张素系统所发挥的作用。方法雄性Wistar大鼠40只,重259.2±17.35g,随机分组,实验组30只,分为A、B和C组各10只。A组单纯皮下注射精蛋白锌胰岛素,B、C组注射同时分别加服心得安和开搏通。所有大鼠注射前、后测血压,注射后留24小时尿测尿纳,尿儿茶酚胺。后心脏取血测血糖,血浆胰岛素,血浆肾素活性和血管紧张素Ⅱ。对照组10只大鼠,皮下注射等量生理盐水。结果 A组血压,C组尿量较对照组显著升高。A、B和C组尿肾上腺素,B、C组尿去甲肾上腺素较对照组显著升高。A、B和C组血糖较对照组显著降低,血浆胰岛素较对照组显著升高。A组血浆肾素活性,血管紧张素Ⅱ均较对照组显著升高,B、C无明显差异。结论 胰岛素诱发大鼠高血压是由肾素-血管紧张素系统活性升高介导的,注射胰岛素后引起低血糖所致交感-儿茶酚胺系统活性增加是肾素-血管紧张素系统活性增加原因之一。     

老年原发性高血压患者瘦素与交感神经活性的关系

目的　探讨瘦素在老年原发性高血压发病机制中的作用。方法　 64例老年原发性高血压患者和 58例对照组人群检测血清瘦素、肾上腺素、去甲肾上腺素、肾素、醛固酮、血管紧张素Ⅱ水平并比较它们之间的关系。结果　高血压组血清瘦素、肾上腺素、去甲肾上腺素水平明显高于对照组 ,差异有显著性。血清瘦素水平与血清肾上腺素、去甲肾上腺素水平呈显著正相关 ,并具有统计学意义。结论　瘦素通过激活交感神经系统参与了老年原发性高血压的发病过程     

心得安和螺旋内酯治疗原发性高血压

本文报告27例原发性高血压病人,随机分配作为期10个月的交叉治疗试验,使用螺旋内酯(200毫克/日),心得安(320毫克/日)和两药半量合用,每期2个月,并间隔服用安慰剂2个月。观察血浆肾素活性的不同反应和二种药物对肾素-血管紧张素-醛固酮系统的不同作用。结果表明,单独使用心得安对大多数原发性高血压病人立位或卧位均有明显降压作用。螺旋内酯对肾素活性低或正常的原发性高血压患者有降压作用。二者对肾素-血管紧张素-醛固酮系统有明显的影响。心得安能降低血浆肾素活性,螺旋内酯则使其加强。心得安的降压效果与治疗前的血浆肾素活性有明显关     

血浆肾素-血管紧张素系统与原发性高血压病的关系评价

目的探究肾素-血管紧张素系统与原发性高血压病的关系。方法选取自2015年以来我院收治的原发性高血压患者50例,其中高血压1级患者18例,2级患者17例,3级患者15例,同时随机选取50例正常健康体检者作为对照,采用放射免疫方法测定所有患者立位、卧位的血浆肾素活性、醛固酮浓度以及血管紧张素浓度,记录并作出比较。结果原发性高血压患者的立位、卧位血浆肾素活性均低于对照组,而立位、卧位的血浆醛固酮浓度以及血管紧张素浓度要高于对照组,并且随着病情的发展,这种差距逐渐增大,差异具有统计学意义(P0.05)。结论肾素-血管紧张素系统与原发性高血压有很密切的关系,其中的指标如血浆肾素活性、血管紧张素浓度、醛固酮浓度等可以作为原发性高血压并诊断、分型及分级的有效指标,同时血浆中的血管紧张素及醛固酮含量的降低也应该作为治疗原发性高血压的重要因素受到临床的重视。     

Effects of the Calcium Antagonist Felodipine on the Sympathetic and Renin-Angiotensin-Aldosterone Systems in Essential Hypertension

ABSTRACT Studies were performed in 10 male patients with untreated essential hypertension, WHO grade I-II, aged 25–62 years, to explore the acute (single dose) and long-term (8 weeks) effects of felodipine on sympathetic activity—evaluated by plasma and urinary catecholamines—as related to blood pressure, heart rate and the activity in the renin-angiotensin-aldosterone system. The patients were hospitalized for 8 (acute) and 6 (long-term) days and were maintained on a standardized daily intake of sodium (150 mmol), potassium (75 mmol) and water (2500 ml). Acute felodipine administration (10 mg) significantly reduced blood pressure and increased heart rate. Plasma and urinary noradrenaline, plasma renin activity and angiotensin II increased, whereas plasma and urinary adrenaline, dopamine, aldosterone and plasma vasopressin were unaltered. Long-term felodipine treatment, 10 mg twice daily, reduced blood pressure to a similar extent as acute felodipine administration, but heart rate was not significantly changed. Plasma noradrenaline 3 and 12 hours after the last dose and urinary noradrenaline were increased, whereas plasma and urinary adrenaline and dopamine were unchanged. Plasma renin activity and angiotensin II were increased 3 hours, but unchanged 12 hours after the last dose. Plasma aldosterone was unchanged but urinary aldosterone increased. Plasma vasopressin was unchanged. The changes in plasma noradrenaline as related to blood pressure, heart rate, plasma renin activity and angiotensin II during long-term felodipine treatment may reflect decreased cardiac and renal β-adrenoceptor-mediated responses. Increased renal clearance of aldosterone could partly explain the unaltered plasma aldosterone level in spite of increased plasma angiotensin II following long-term felodipine treatment.     

依那普利对心力衰竭患者血压及交感活性的影响

目的 研究不同剂量依那普利治疗后,在不同血压水平对充血性心力衰竭患者交感神经活性的影响.方法 选取2012年1月至2013年4月在江苏省泰兴市人民医院住院的心力衰竭患者,在未服降压药物的情况下,血压110/70 mm Hg（1 mm Hg=0.133 kPa）以上,纽约心脏协会心功能Ⅲ级或不必卧床的Ⅳ级.所有患者在入院时进行病史资料采集,并检测血浆肾上腺素、去甲肾上腺素、肾素、血管紧张素Ⅱ、醛固酮浓度.入选后予依那普利口服,起始剂量5 mg/d,根据血压情况,逐渐加量至10 mg/d.三周后按平均收缩压≥100 mm Hg和＜100 mm Hg分为A组和B组.对于A组患者,从第4周开始,增加药物剂量,至平均收缩压＜100 mmHg,并维持至第6周.B组患者继续原治疗方案至第6周.在第3周和第6周分别进行上述神经内分泌因子活性检测,比较不同时间段两组神经内分泌因子的活性.结果 48例患者入选,其中A组26例,B组22例.两组治疗前临床特点、交感活性及治疗后左心室射血分数比较,差异无统计学意义（P＞0.05）.治疗6周后,A组血管紧张素转换酶抑制剂（ACEI）剂量较B组大,差异有统计学意义[（14.3±4.5） mg vs.（7.5±2.4） mg,P＜0.05].两组肾上腺素、去甲肾上腺素浓度比治疗前显著降低,差异有统计学意义[A组肾上腺素：（256.1±77.3） pg/mL vs.（168.7±53.3）,P＜0.05;A组去甲肾上腺素：（1 734±534） pg/mL vs.（844±399） pg/mL,P＜0.05;B组肾上腺素：（248.7±62.3） pg/mL vs.（218.1±60.3） pg/mL,P＜0.05;B组去甲肾上腺素（1 645±619）pg/mL vs.（1 084±431） pg/mL,P＜0.05],且A组下降更明显.两组治疗前后血浆肾素、血管紧张素、醛固酮变化不明显,差异无统计学意义（P＞0.05）.结论 血管紧张素转换酶抑制剂治疗后,达到相同目标血压时,较大治疗剂量患者交感活性下降明显,而治疗剂量较小者交感活性虽有下降,但下降幅度小,提示对于后者应当采取各种措施进一步降低交感活性.     

Effects of adding spironolactone to an angiotensin-converting enzyme inhibitor in chronic congestive heart failure secondary to coronary artery disease

In chronic heart failure, a diuretic plus an angiotensin-converting enzyme (ACE) inhibitor only partially suppresses aldosterone despite the fact that aldosterone has many harmful effects independent of angiotensin II. These possible harmful effects of aldosterone are magnesium loss, increased cardiac sympathetic activity, and increased ventricular arrhythmias. We have therefore assessed whether adding the aldosterone antagonist, spironolactone, to a loop diuretic and ACE inhibitor reverses any of these potentially harmful effects of residual aldosterone. In a preliminary animal study, we found that exogenous aldosterone reduced myocardial norepinephrine uptake by 24% in anesthetized rats in vivo. In our main study, 42 patients with New York Heart Association II to III congestive heart failure were randomized to spironolactone (50 to 100 mg/ day, titrated to blood pressure and plasma potassium) or placebo in a double-blind fashion. Our principal finding is that cardiac norepinephrine uptake as assessed by ¹²³I-metaiodobenzylguanidine scintigraphy increased with spironolactone (p < 0.01). Spironolactone also elevated plasma magnesium (p < 0.05), reduced urinary magnesium excretion (p < 0.05), and caused a reduction in ventricular arrhythmias on 24-hour ambulatory electrocardiography (p < 0.05). Spironolactone increased plasma renin activity, plasma aldosterone (p < 0.01), 24-hour urinary sodium excretion (p < 0.05), and urinary sodium/potassium ratio (p < 0.01). Echocardiographic-determined measurements of left ventricular systolic and diastolic function were unaltered by spironolactone. Therefore, spironolactone has potentially beneficial effects on cardiac adrenergic tone, divalent cation balance, and ventricular arrhythmias in patients with chronic heart failure who are already receiving standard doses of ACE inhibitors. All of these factors could be significant in the prevention of sudden cardiac death in this population.     

Endothelin-1 and Adrenomedullin Plasma Levels After Exposure to Fludrocortisone,Dexamethasone, and Spironolactone

We asked whether plasma concentrations of endothelin-1 (ET-1) or adrenomedullin (ADM) are altered by different activity states of the renin–angiotensin–aldosterone system (RAAS). Levels of ET-1 and ADM were studied in patients with primary aldosteronism (n = 15), essential hypertension (n = 15), and adrenal insufficiency (n = 7). Effects of fludrocortisone, dexamethasone, or spironolactone treatment on ET-1 and ADM levels were also analyzed. Plasma ET-1 and ADM concentrations did not differ significantly between the patient groups. After fludrocortisone, dexamethasone, or spironolactone treatment, both ET-1 and ADM did not change significantly. The data support the hypothesis that the RAAS is not directly linked with the ET-1/ADM system.     

收缩性心力衰竭兔神经激素的变化研究

目的 探讨兔收缩性心力衰竭(systolic heart failure,SHF)的血浆神经激素脑钠肽(BNP)、去甲肾上腺素(NE)、肾上腺素(EPI)、血管紧张素Ⅱ(AngⅡ)的变化.方法 将40只新西兰大白兔随机分为两组:SHF组(行腹主动脉缩窄联合主动脉瓣毁损术)、假手术组(行假手术),通过超声心动图和血流动力学检查心功能的改变,第12周抽血检查血浆BNP、NE、EPI、AngⅡ水平.结果 与假手术组相比,SHF组左室腔明显增大,收缩功能显著下降,血浆BNP、NE、EPI、AngⅡ水平较假手术组明显升高(P＜0.01).结论 SHF组的神经激素水平明显增高.     

Determinants of increased angiotensin II levels in severe chronic heart failure patients despite ACE inhibition

INTRODUCTION: The beneficial effects of ACE inhibitors are generally ascribed to blockade of neurohormonal activation. However, especially in chronic heart failure (CHF) patients plasma angiotensin II and aldosterone levels can be elevated despite ACE inhibition, the so-called ACE escape. In the present study, we aimed to identify the frequency and determinants of ACE escape in CHF patients. METHODS: We studied 99 stable chronic heart failure patients (NYHA class III and IV, 66% ischemic etiology) receiving long-term therapy with ACE inhibitors. In all patients, cardiac, renal, and neurohormonal parameters were measured. ACE escape was defined as plasma angiotensin level > or = 16 pmol/L. RESULTS: Mean (+/- SD) left ventricular ejection fraction of our 99 patients (79 men and 20 women, age 69 +/- 12 years) was 28 +/- 10%. In addition to an ACE inhibitor, 93% of patients received diuretics, 71% a beta-blocker, and 49% spironolactone. None of the patients used an angiotensin receptor blocker. In our population, 45% of the patients had an angiotensin II plasma concentration higher than 16 pmol/L (median concentration was 14.1 pmol/L). Spironolactone use was an independent predictor of elevated plasma angiotensin II levels. Furthermore, spironolactone users had significantly higher plasma active renin protein and aldosterone levels. Plasma angiotensin II concentration was positively correlated to active renin, plasma angiotensin I and plasma aldosterone. No correlation was found between plasma angiotensin II levels and serum ACE activity, dose of ACE inhibitor, or duration of use. CONCLUSION: In a group of severe chronic heart failure patients, 45% had elevated plasma angiotensin II levels independent of serum ACE activity despite long-term ACE inhibitor use. Although a causal link could not be proven, an association was found between spironolactone use and active renin protein, angiotensin II and aldosterone levels, suggesting that escape from ACE is mainly caused by a feedback mechanism.     

Controlled treatment of primary hypertension with propranolol and spironolactone: A crossover study with special reference to initial plasma renin activity

Twenty-seven patients with hypertension were randomly allocated to a 10 month crossover study. Treatment consisted of spironolactone (200 mg/day for 2 months), propranolol (320 mg/day for 2 months) and combined administration of both drugs at half the dosage. Between treatment periods placebo was given for 2 months. Fourteen patients were previously untreated. The average pretreatment blood pressure for the entire group was 188/114 ± 16/7 (mean ± standard deviation) mm Hg supine and 188/118 ± 20/9 mm Hg standing. Both spironolactone and propranolol reduced blood pressure significantly in both the supine and standing positions.Upright plasma renin activity was determined by radioimmunoassay of angiotensin I. The average initial level was 1.9 ± 1.2 (range 0.4 to 5.0) ng/ml/hr. There was a close correlation between plasma renin activity and the effects of the drugs: With increasing renin level the response to propranolol was better whereas the opposite was true for spironolactone. The combination of spironolactone and propranolol decreased the blood pressure still further in the supine and standing positions, irrespective of initial plasma renin activity. All patients achieved a normal supine pressure. Blood pressure and plasma renin activity returned toward pretreatment values during placebo administration. It is concluded that pretreatment levels of plasma renin activity can predict the antihypertensive response to propranolol and spironolactone. The combination of the two drugs, which have different modes of action, will effectively reduce blood pressure in hypertension. The results support the concept that the renin-angiotensin-aldosterone system may be involved in primary hypertension.