肾静脉肾素测定预测肾动脉狭窄介入治疗后血压变化价值的探讨

肾动脉狭窄（RAS）常表现为肾血管性高血压（RVH）和缺血性肾病，65岁以上老年人中的发病率不低于7%［1］。近年来经皮腔内肾血管成形及支架植入术已广泛应用于RAS的治疗［2］，但并不是所有RAS患者都能从介入治疗中获益，大约70%患者术后血压改善甚至治愈［3］。为此，需要预测介入手术术后血压变化并选择可以从中获益的患者。RVH由肾素-血管紧张素-醛固酮系统（RAAS）激活引起［4］，过去认为肾静脉肾素（PRA）活性测定可以作为评估介入手术后血压变化的指标［5］，目前对此存有争议。本文采用临床高度怀疑RAS的患者行肾动脉造影，并测定肾静脉及下腔静脉PRA，观察动态血压，藉以评价PRA测定对预测介入治疗后血压变化有无临床意义。     

静脉自控镇痛对高血压病患者肾素-血管紧张素及心钠素的影响

目的：观察曲马多复合芬太尼静脉自控镇痛对高血压病患者肾素-血管紧张素系统及心钠素的影响。 方法：于2004-12／2005-12选择泸州医学院附属医院骨科有1年原发性高血压病史并择期行股骨头置换术或股骨骨折内固定术的患者40例为观察对象。随机数字表法分为对照组和静脉自控镇痛组，每组20例。患者均知情同意并自愿参加。所有病例在手术过程中均采用静吸复合全麻。对照组患者术毕回病房常规镇痛，当患者自述疼痛难忍时肌注哌替啶50mg／次。静脉自控镇痛组患者清醒拔管后开始行静脉自控镇痛。术毕静脉给予曲马多100mg＋盐酸格拉司琼3mg为负荷量。静脉自控镇痛液配方为曲马多900mg＋芬太尼0．3mg＋盐酸格拉司琼3mg加生理盐水稀释至150mL。采用放免法测定术前、术毕、术后24，48h血浆肾素活性，血管紧张素Ⅱ及心钠素浓度；监测心率、血压；并进行术后8，12，24及48h的目测类比评分比较。 结果：所有患者均完成手术，并进入结果分析。（1）两组高血压患者术前肾素活性，血浆血管紧张素Ⅱ及心钠素值分别高于正常参考值[肾素活性：（0．42&;#177;0．37）mg／（L&;#183;h），血浆血管紧张素Ⅱ：（40．2&;#177;12．0）ng／L，心钠素：（379．00&;#177;76．60）ng／L]。静脉自控镇痛组患者术毕、术后24，48h时肾素活性、血浆血管紧张素Ⅱ低于术前；术毕、术后24h时肾素活性、血浆血管紧张素Ⅱ值显著低于对照组。对照组患者术毕、术后24h的心钠素高于术前，而静脉自控镇痛组患者术后各时点心钠素差异无显著性意义。静脉自控镇痛组术毕、术后24h心钠素值显著低于对照组（P〈0．05）。（2）对照组患者术后8，12，24，48h的目测类比评分显著低于静脉自控镇痛组，差异有显著性意义。（3）静脉自控镇痛组术毕、术后24h时由于疼痛缓解，收缩压低于对照组（P〈0．01），两组患者术后48h收缩压差异无显著性意义。 结论：术后曲马多复合芬太尼静脉自控镇痛，能有效减轻患者疼痛，抑制应激反应，降低高血压患者骨科手术后肾素活性，血管紧张素Ⅱ及心钠素值，维持血液动力学稳定。     

两种透析方式对顽固性高血压及血管活性物质的影响

目的：比较腹膜透析（CAPD）和血液透析（IHD）对尿毒症患者顽固性高血压的影响及对其肾素活性、内皮素、血管紧张素Ⅱ清除率的影响。方法：符合入选标准的50例尿毒症并顽固性高血压的患者随机分为CAPD组和IHD组,记录患者治疗前后肌酐（Cr）,尿素氮（BUN）、血红蛋白（Hb）、血球压积（Hct）、肾素活性（RA）、内皮素（ET）、血管紧张素Ⅱ（AngⅡ）和24 h动态血压的变化,比较两组治疗后的RA、ET、AngⅡ和24 h动态血压。结果：①治疗6个月后两组肌酐,尿素氮,血红蛋白,血球压积均有明显改善（P〈0.05）,但组间比较无显著性差异（P〉0.05）。②治疗6个月后CAPD组24 h平均血压、RA、ET、AngⅡ均有明显改善（P〈0.05）,而IHD组无明显改变（P〉0.05）;组间比较有显著性差异（P〈0.05）。结论：①腹膜透析和血液透析两种透析方式均可以很好的清除尿毒症小分子毒素,改善尿毒症贫血状态和毒素水平。②腹膜透析比血液透析更有利于清除肾素、内皮素、血管紧张素Ⅱ,从而能更好地控制尿毒症顽固性高血压。     

静脉自控镇痛对高血压病患者肾素-血管紧张素及心钠素的影响

目的:观察曲马多复合芬太尼静脉自控镇痛对高血压病患者肾素-血管紧张素系统及心钠素的影响。方法:于2004-12/2005-12选择泸州医学院附属医院骨科有1年原发性高血压病史并择期行股骨头置换术或股骨骨折内固定术的患者40例为观察对象。随机数字表法分为对照组和静脉自控镇痛组,每组20例。患者均知情同意并自愿参加。所有病例在手术过程中均采用静吸复合全麻。对照组患者术毕回病房常规镇痛,当患者自述疼痛难忍时肌注哌替啶50mg/次。静脉自控镇痛组患者清醒拔管后开始行静脉自控镇痛。术毕静脉给予曲马多100mg 盐酸格拉司琼3mg为负荷量。静脉自控镇痛液配方为曲马多900mg 芬太尼0.3mg 盐酸格拉司琼3mg加生理盐水稀释至150mL。采用放免法测定术前、术毕、术后24,48h血浆肾素活性,血管紧张素Ⅱ及心钠素浓度;监测心率、血压;并进行术后8,12,24及48h的目测类比评分比较。结果:所有患者均完成手术,并进入结果分析。①两组高血压患者术前肾素活性,血浆血管紧张素Ⅱ及心钠素值分别高于正常参考值[肾素活性:(0.42±0.37)mg/(L·h),血浆血管紧张素Ⅱ:(40.2±12.0)ng/L,心钠素:(379.00±76.60)ng/L]。静脉自控镇痛组患者术毕、术后24,48h时肾素活性、血浆血管紧张素Ⅱ低于术前;术毕、术后24h时肾素活性、血浆血管紧张素Ⅱ值显著低于对照组。对照组患者术毕、术后24h的心钠素高于术前,而静脉自控镇痛组患者术后各时点心钠素差异无显著性意义。静脉自控镇痛组术毕、术后24h心钠素值显著低于对照组(P<0.05)。②对照组患者术后8,12,24,48h的目测类比评分显著低于静脉自控镇痛组,差异有显著性意义。③静脉自控镇痛组术毕、术后24h时由于疼痛缓解,收缩压低于对照组(P<0.01),两组患者术后48h收缩压差异无显著性意义。结论:术后曲马多复合芬太尼静脉自控镇痛,能有效减轻患者疼痛,抑制应激反应,降低高血压患者骨科手术后肾素活性,血管紧张素Ⅱ及心钠素值,维持血液动力学稳定。     

血管紧张素Ⅱ受体阻断剂对慢性肾脏病患者肾素-血管紧张素系统表达的影响

目的：研究血管紧张素Ⅱ受体阻断剂（angiotensinⅡ receptor blocker,ARB）对慢性肾脏病（chronic kidney disease,CKD）患者循环和肾脏肾素-血管紧张素系统（renin-angiotensin system,RAS）表达的影响。方法：行肾脏活组织检查且2个月内未曾服用血管紧张素转换酶抑制剂的CKD患者,其中2周内ARB治疗的患者17例（ARB治疗组）,另选取2周内未应用ARB治疗的患者17例（空白对照组）,根据年龄、性别、血压、估算肾小球滤过率（eGFR）、24h尿蛋白、尿钠等进行配对。采用放射免疫法和酶联免疫吸附分析（ELISA）方法测定血、尿RAS组分的浓度,并采用免疫组织化学方法评价肾脏肾素、血管紧张素原（AGT）、血管紧张素Ⅱ（AngⅡ）和血管紧张素Ⅱ受体的表达。分析ARB对血、尿和肾组织RAS表达的影响。结果：ARB治疗组与空白对照组在性别、年龄、eGFR、24h尿蛋白、尿钠和血压等方面均显著差异。ARB治疗组血浆AngⅡ高于空白对照组[（63.09±15.14）pg/mL比（53.66±8.33）pg/mL,P〈0.05],肾内肾素免疫组织化学染色面积高于空白对照组[（48.65±19.58）%比（30.29±24.98）%,P〈0.05]。ARB治疗组肾内AGT、AngⅡ和血管紧张素Ⅱ1型受体免疫组织化学染色面积略低于空白对照组,但差异无统计学意义。结论：ARB治疗对循环和肾脏局部RAS表达的影响不同,可使循环AngⅡ升高,并可能抑制肾脏局部AngⅡ的表达。     

血液透析滤过治疗尿毒症难治性高血压的临床观察

目的：探讨治疗尿毒症难治性高血压的有效方法。方法：将50例尿毒症行维持性血液透析的难治性高血压患者分为对照组和实验组各25例,对照组采用常规血液透析,每周2～3次。实验组采用常规血液透析的同时接受血液透析滤过,每周行血液透析2次,血液透析滤过1次。分别观察两组患者治疗前、治疗3个月后血压及血浆肾素、血管紧张素Ⅱ浓度的变化。结果：对照组治疗前后血压及血浆肾素及血管紧张素Ⅱ浓度比较无统计学意义（P〉0．05）;实验组治疗前后血压及血浆肾素、血管紧张素Ⅱ浓度比较有显著性差异（P〈0．01）;两组治疗后血压及血浆肾素、血管紧张素Ⅱ浓度比较有显著性差异（P〈0．01）。结论：尿毒症难治性高血压在常规血液透析治疗的同时接受血液透析滤过能有效的清除血浆肾素、血管紧张素,从而降低血压,增强了透析效率,减少了并发症的发生,提高了患者的生活质量。     

糖尿病大鼠肾组织核因子κB活性与血管紧张素系统的关系

背景：目前已知血管紧张素Ⅱ在糖尿病肾病发病中起重要作用。因此。核因子KB对糖尿病大鼠肾组织血管紧张素系统可能有调节作用。 目的：观察抑制核因子KB活性与糖尿病大鼠肾组织血管紧张素Ⅱ及其1型受体mRNA表达的关系。 设计：完全随机分组设计，对照实验。 材料：实验于2000-03／04在中山医科大学实验动物中心完成。选用51只纯种清洁级雄性Wistar大鼠。 方法：①对其中39只大鼠进行造模，采用链脲佐菌素溶于枸橼酸缓冲液（0．1mmol／L，pH=4．5），按60mg／kg腹腔内注射，制备糖尿病模型，空腹血糖维持在13．9mmol／L以上则模型制备成功。随机将造模后39只大鼠分为3组：模型组（n=17，未给予其他干预措施，正常饲养）和吡咯烷二硫基甲酸酯（核因子κB活性抑制剂）干预组[n=22，腹腔内注射吡咯烷二硫基甲酸酯（剂量20mg／kg），2次／d]。其余12只为正常对照组。未造成糖尿病模型，正常饲养。②各组饲养18周后取出肾脏，电泳迁移率变动分析技术检测核因子κB活性，采用反转录聚合酶链反应法检测血管紧张素Ⅱ 1型受体mRNA表达，采用放射免疫分析法检测血管紧张素Ⅰ与血管紧张素Ⅱ含量。37℃水浴后的血管紧张素Ⅰ水平减去4℃检测的血管紧张素Ⅰ水平则为肾素活性。③计量资料差异性比较采用单因素方差分析，非正态分布资料经正态转换后再作统计学处理。 主要观察指标：各组大鼠肾组织血管紧张素Ⅰ，Ⅱ含量和肾素、核因子κB活性及血管紧张素Ⅱ 1型受体mRNA表达比较。 结果：正常对照组、模型组、吡咯烷二硫基甲酸酯干预组大鼠各脱失1，6，13只，进入结果分析11，11，9只。①核因子κB活性：模型组明显高于正常对照组和吡咯烷二硫基甲酸酯干预组（P〈0．01），正常对照组与吡咯烷二硫基甲酸酯干预组相近。②肾组织肾素活性：3组相近。③肾组织血管紧张素Ⅰ含量：模型组明显高于正常对照组和吡咯烷二硫基甲酸酯组（P〈0．01）。④肾组织血管紧张素Ⅱ含量：模型组与正常对照组相近，吡咯烷二硫基甲酸酯组明显低于模型组和正常对照组（P〈0．01）。血管紧张素Ⅱ 1型受体mRNA表达：模型组明显低于正常对照组（P〈0．01）；吡咯烷二硫基甲酸酯组明显低于模型组和正常对照组（P〈0．01）。 结论：糖尿病大鼠肾组织核因子κB活性增加，抑制核因子κB活性后可导致糖尿病大鼠肾组织血管紧张素Ⅱ水平及血管紧张素Ⅱ 1型受体mRNA表达下降。     

促肾上腺激素、肾素、血管紧张素Ⅱ、醛固酮、皮质醇联合检测在高血压诊治中的临床应用研究

目的探讨促肾上腺激素、肾素、血管紧张素Ⅱ、醛固酮、皮质醇联合检测在高血压诊治中的临床价值。方法选取我院2017年1月～2018年6月收治的原发性高血压患者50例作为原发性高血压组,50例肾性高血压患者为肾性高血压组,另选取同期健康体检者50例为对照组。在患者入院时及入院接受治疗后使用安图化学发光AutO2000检测促肾上腺激素、肾素、血管紧张素Ⅱ、醛固酮、皮质醇五项血清指标,比较各组血清指标水平;采用Spearman相关性分析血清促肾上腺激素、肾素、血管紧张素Ⅱ、醛固酮、皮质醇水平与患者动态血压相关指标的相关性;采用受试者操作特性曲线(ROC)分析血清促肾上腺激素、肾素、血管紧张素Ⅱ、醛固酮、皮质醇水平的联合检测对原发性高血压、肾性高血压组及预后的诊断评估中的价值,分别计算其敏感度、特异度。结果肾性高血压组、原发性高血压组与对照组比较,各项血清指标均升高,且肾性高血压组各项血清指标均高于原发性高血压组,差异有统计学意义(P0.05);治疗后肾性高血压组、原发性高血压组患者各项血清指标较治疗前均显著降低,差异有统计学意义(P0.05);治疗前,两组高血压患者动态血压相关指标比较,差异无统计学意义(P0.05),治疗后血压指标较治疗前均降低,但明显高于对照组,差异有统计学意义(P0.05);Pearson相关分析显示,各项血清水平与患者动态血压相关指标呈正相关关系(P0.05);ROC曲线分析结果显示,血清促肾上腺激素、肾素、血管紧张素Ⅱ、醛固酮、皮质醇联合检测对高血压的诊断价值良好,均有较高的敏感度、特异度(P0.05)。结论高血压患者促肾上腺激素、肾素、血管紧张素Ⅱ、醛固酮、皮质醇水平较明显升高,联合检测血促肾上腺激素、肾素、血管紧张素Ⅱ、醛固酮、皮质醇水平对高血压患者的诊断及预后评估价值良好。     

厄贝沙坦联合阿魏酸哌嗪治疗慢性肾衰竭疗效分析

目的观察厄贝沙坦联合阿魏酸哌嗪治疗慢性肾衰竭（CRF）的疗效。方法将80例CRF患者随机分为治疗组和对照组。治疗组给予厄贝沙坦和阿魏酸哌嗪;对照组给予β受体阻滞剂等降压药,均未服用肾素-血管紧张素转换酶抑制剂（ACEI）或血管紧张素Ⅱ受体拮抗剂（ARB）。观察患者血压、蛋白尿、血尿素氮（BUN）、血肌酐（Scr）的数值变化情况。结果两组治疗后血压均有下降;治疗组蛋白尿、BUN、Scr水平均较对照组下降明显,差异有统计学意义（P〈0.05）。结论厄贝沙坦联合阿魏酸哌嗪可以改善肾功能,延缓CRF进展。     

解毒通络保肾胶囊对糖尿病大鼠肾脏的保护作用

背景：临床观察发现中药解毒通络保肾胶囊对糖尿病肾病具有较好的防治作用,但具体作用途径不甚清楚.目的：探讨解毒通络保肾胶囊对糖尿病大鼠肾脏病变的保护作用及其机制.设计：随机对照观察.单位：吉林大学再生医学科学研究所及长春中医学院中医研究所.材料：实验于2002-05/2003-01在吉林大学再生医学科学研究所病理研究室完成.选用Wistar大鼠46只.方法：将实验动物分为正常对照组（10只）;糖尿病对照组（12只）;苯那普利治疗组（阳性对照组,12只）和解毒通络保肾胶囊治疗组（实验组,12只）.检测各组第12周的血糖、尿素氮、血肌酐、尿白蛋白排泄率、肾组织的肾素活性、血管紧张素转换酶活性、血管紧张素Ⅱ含量和肾脏肥大指标及肾脏组织学检查,应用反转录-聚合酶链反应检测肾皮质转化生长因子β1mRNA表达水平,免疫组化法检测肾脏纤维连接蛋白和Ⅳ型胶原蛋白表达水平.主要观察指标：①糖尿病和糖尿病肾病相关的生化指标检测.②肾脏组织的肾素活性、血管紧张素转换酶和血管紧张素Ⅱ水平.③肾脏纤维连接蛋白、兔抗鼠Ⅳ型胶原蛋白表达水平.④肾皮质转化生长因子β1mRNA表达.⑤组织学观察.结果：在实验过程中糖尿病对照组死亡5只大鼠,阳性对照组和实验组大鼠分别死亡4只和3只.实验结束时,正常对照组、糖尿病对照组、阳性对照组和实验组分别有10,7,8,9只进入结果分析.①糖尿病和糖尿病肾病相关的生化指标检测：阳性对照组和实验组与糖尿病对照组比较,体质量上升、肾重/体质量和血糖降低（P＜0.05,P＜0.01）,实验组血糖较糖尿病对照组和阳性对照组下降明显（P＜0.01）.阳性对照组和实验组的尿素氮、血肌酐、内生肌酐清除率和尿白蛋白排泄率指标均较糖尿病对照组显著下降（P＜0.05,P＜0.01）.②肾脏组织的肾素活性、血管紧张素转换酶和血管紧张素Ⅱ水平：阳性对照组肾组织肾素活性较其余3组明显升高（P＜0.01）.阳性对照组和实验组肾组织中血管紧张素转换酶活性和血管紧张素Ⅱ含量较糖尿病对照组明显下降（P＜0.01）,其中血管紧张素转换酶活性阳性对照组较实验组下降明显（P＜0.05）.③肾脏纤维连接蛋白、兔抗鼠Ⅳ型胶原蛋白表达水平：阳性对照组和实验组较糖尿病对照组免疫染色明显减弱（P＜0.01）,介于正常对照组和糖尿病对照组之间.④肾皮质转化生长因子β1mRNA表达：阳性对照组和实验组的表达水平较糖尿病对照组显著下降,分别为糖尿病对照组的66.28%,64.75%（P＜0.05）.⑤组织学观察：光镜下阳性对照组和实验组大鼠肾小球系膜增生、肾小球基底膜增厚均较轻,且系膜区扩大不明显,肾小球基底膜无明显增厚且厚度均匀,系膜细胞增多不显著,上皮细胞足突均匀分布.结论：解毒通络保肾胶囊对糖尿病肾脏病变有保护作用,其机制可能是通过抑制肾组织肾素活性和血管紧张素转换酶,减少肾组织中血管紧张素Ⅱ含量,下凋糖尿病大鼠肾皮质转化生长因子β1 mRNA表达,减少细胞外基质的沉积.     

Aspirin injection test to predict angioplasty outcome in unilateral renovascular hypertension: preliminary report.

We examined the usefulness of aspirin DL-lysine for prediction of the outcome of renal artery angioplasty in renovascular hypertension. The study was carried out in eight hypertensive patients with unilateral renal artery stenosis: six were free from azotemia and two had slight azotemia. Before and 30 min after an intravenous injection of aspirin DL-lysine (18 mg/kg), renal venous and abdominal aortic plasma was sampled and assayed for prostaglandin E2 and plasma renin activity. Blood pressure and heart rate were serially measured at this time. Renal angioplasty was later performed and was technically successful in all patients. In the six patients without azotemia, aspirin inhibited renal prostaglandin E2 synthesis and suppressed renin release from the ischemic kidney, resulting in lowered blood pressure. Renal angioplasty caused plasma renin activity to become normal and lowered high blood pressure. The reduction in blood pressure by angioplasty was correlated with the responses of blood pressure and renin release to aspirin. However, in the two patients with azotemia, aspirin neither suppressed renin release nor lowered blood pressure. Their hypertension was not reduced by the angioplasty. These results indicate that an aspirin injection test could be useful for prediction of the outcome of angioplasty in unilateral renovascular hypertension.     

Hypertension Following Renal Transplantation: The Role of the Host's Kidneys

Renin, aldosterone and exchangeable sodium were measured in38 hypertensive and 56 normotensive renal transplant recipientswith good renal function and without renal artery stenosis.Response to competitive blockade of angiotensin II using saralasinwas studied in 20 of the hypertensive group. Hypertension was uncommon when bilateral nephrectomy had beenperformed. When diseased kidneys remained in situ, blood pressureafter transplantation correlated well with blood pressure ondialysis. Plasma renin activity was higher in hypertensive patients despitehigher exchangeable sodium levels. Urinary aldosterone was alsohigher and correlated well with blood pressure and plasma reninactivity. Angiotensin II blockade produced a fall in blood pressureproportional to plasma renin activity. These observations suggest that hypersecretion of renin is anaetiological factor in the hypertension of renal transplantrecipients. It appears to act both through the stimulation ofaldosterone secretion, with resultant salt retention, and throughthe direct vasoconstrictor action of angiotensin II. Since reninlevels were lower in patients subjected to bilateral nephrectomythe source of the excess renin is probably the host's kidneys.     

Renal Artery Stenosis Presenting with Status Epilepticus: A Report of One Case

In children, renal artery stenosis is an uncommon but important cause of secondary hypertension. In this report, the authors describe a 5-year-old boy with no history of seizures who experienced status epilepticus. Postictal blood pressure, relative hypotension, was misinterpreted as normal on the day of admission. Two days later, his blood pressure rose gradually and peripheral plasma renin activity showed more than 1,700 micro U/mL. Magnetic resonance angiography suggested renal artery stenosis. After successful percutaneous transluminal angioplasty, the patient was seizure-free and had well-controlled blood pressure. This case describes renal artery stenosis present with status epilepticus, and emphasizes the importance of serial measurements of blood pressure in children.     

待肾源移植透析者连续性肾脏替代治疗对顽固性高血压的影响

背景：维持性血液透析人群中有10%-49%的患者合并顽固性高血压,常规药物治疗效果差。连续性肾脏替代治疗可较好地清除患者血浆中的中、大分子毒素,理论上可通过降低相关毒素水平干预顽固性高血压形成机制。 目的：观察连续性肾脏替代治疗对维持性血液透析患者顽固性高血压的影响。 方法：45例维持性血液透析合并顽固性高血压患者,随机分为血液透析组22例与连续性血液净化组23例,血液透析组则行常规血液透析治疗,连续性肾脏替代治疗组在常规血液透析治疗基础上每周行连续性肾脏替代治疗1次。 结果与结论：治疗3个月后,连续性血液净化组肾素、内皮素、血管紧张素Ⅱ、C-反应蛋白、白细胞介素6、肿瘤坏死因子α水平均低于试验前水平,24 h平均血压下降,且差异均有显著性意义（P＜0.05）,血液透析组上述各指标较试验前无变化（P＞0.05）;试验后连续性血液净化组上述各指标均低于血液透析组,差异有显著性意义（P＜0.05）。结果显示在常规血液透析基础上行连续性肾脏替代治疗可明显降低合并顽固性高血压维持性血液透析患者的血压,其机制可能是降低了患者血浆中的中、大分子毒素以及炎症因子水平。     

Role of the renin-angiotensin system in hypertension after coarctation of the aorta

The effect of inhibition of angiotensin I converting enzyme by captopril was studied in rats with aortic coarctation produced above the renal arteries. When captopril therapy was started before coarctation, blood pressure above the narrowing and the pressure difference across the coarctation were reduced, compared with values in animals with coarctation not given therapy. When captopril therapy was started 10 days after the coarctation, there was no effect on blood pressure. Plasma renin activity increased 24 hours after coarctation and returned to control levels by 5 days. Captopril caused an increase in renin activity and a decrease in plasma aldosterone concentrations. After 5 days, there was no difference in renin activity and plasma aldosterone levels between animals with coarctation given captopril therapy early and late and between appropriate controls. Our data suggest that the renin-angiotensin system is important in the early development but not in the maintenance of coarctation hypertension.     

Renal artery occlusive disease

Renal artery occlusive disease, from either atherosclerosis or fibrous dysplasia, may cause hypertension or renal insufficiency. Hypertension results from increased activity of the renin-angiotensin-aldosterone system. There are several ways to evaluate this system as well as several pharmacologic agents that will intervene and modulate the hypertension that results. Percutaneous transluminal angioplasty or surgical revascularization will be necessary in some patients to control blood pressure or improve renal function. Successful evaluation and treatment of these patients are based on clinical experience, an understanding of the natural history of the various disease processes involved, and a comprehensive team approach.     

Effect of enalapril on renin, angiotensin converting enzyme activity, aldosterone and prostaglandins in patients with hypertension

Enalapril (MK-421) was administered orally as a single dose of 2.5, 5.0, 10 and 20 mg to 13 patients with either essential or renovascular hypertension. At these doses, enalapril produced a moderate reduction in both supine and standing blood pressure as well as a significant reduction in angiotensin I-converting enzyme activity, an increase in peripheral plasma renin activity and a decrease in plasma aldosterone concentration 4 to 8 hours after administration of the drug. Plasma levels of prostaglandins E1 and E2 were unchanged. The calculated ratio of urinary Na/K was increased in the patients with renal artery stenosis after enalapril. Creatinine clearance was increased in the patients with essential hypertension and reduced in the patients with renal artery stenosis. No adverse effects occurred in these patients treated with single doses of enalapril.     

Renin Activation in the Venous Plasma from the Involved Kidney in the Patient with Renal Hypertension

Measurements of plasma renin activity (PRA) in renal vein blood from the ischemic kidney are reported to be generally higher than from the contralateral kidney. Importance of factors other than renin content of renal venous plasma has not been investigated. Initial rate measurements of angiotensin generation with added excess of homologous renin (Plasma Renin Substrate Activity [PRSA]-20 min) were made in bilateral renal venous plasma from 31 patients suspected of suffering from unilateral renal hypertension. The mean values from the involved vs. the contralateral kidney were 551 vs. 331 ng respectively of angiotensin II equivalents generated per milliliter of plasma per 20 min of incubation. The measurement of maximal angiotensin generation under the same conditions with incubation prolonged to 3 hr (PRSA-180 min), however, were bilaterally equal in renal venous plasma from selected patients with renal hypertension who showed distinct differences in PRSA-20 min and PRA measurements. Prior extraction of plasma lipids did not significantly change the bilateral renal venous PRSA-20 min determinations. Stimulation of endogenous renin release in normal dogs did not change the PRSA determinations. The data suggest strongly the presence of a "renin activating" mechanism in the renal venous plasma from the involved kidney of patients with renal hypertension.     

Management of atherosclerotic renal artery stenosis

The management of atherosclerotic renal artery stenosis is controversial. Although it may appear intuitive that restoring normal blood flow to the kidney(s) is the treatment of choice, there are no data showing an obvious advantage of interventional therapy compared with medical therapy. In this article, we discuss the most recent advances in the treatment of atherosclerotic renal artery stenosis with a focus on randomized studies comparing medical treatment with angioplasty/stenting, particularly in patients with underlying renal dysfunction. The available data are still of limited quality but provide support against indiscriminate use of interventions, as these treatments appear no better than best medical treatment that focuses on blood pressure control, use of blockers of the renin–angiotensin system, and aggressive cardiovascular risk management.     

Renal extraction of angiotensin II

Angiotensin II regulates many aspects of renal function and thereby influences long-term blood pressure. The effects of angiotensin II on the kidney have been exhaustively studied; however, the converse (i.e., effects of the kidney on angiotensin II) has received little attention. Accordingly, the focus of this study was to determine whether renal degradation of angiotensin II is regulated by chronic levels of angiotensin II or long-term levels of blood pressure. Twenty hypertensive rats and 22 normotensive rats were treated for 1 week with either vehicle, angiotensin II (50 ng/kg/min, subcutaneously) or captopril (100 mg/kg/day, orally). Right kidney vascular resistance was measured during infusions of angiotensin II into the left renal artery or vena cava at the level of left renal vein. Dose-response data were curve-fitted, and the extraction of angiotensin II by the left kidney was calculated by comparing the doses of angiotensin II required to elicit equal increases in right renal vascular resistance during intravenous versus left intrarenal artery infusions. Renal extraction of angiotensin II was high (mean, 81%) and demonstrated little animal-to-animal variation (coefficient of variation, 23%; standard deviation, 19%). Renal extraction of angiotensin II was independent of hypertension (P = 0.257) or previous chronic exposure to angiotensin II or captopril (P = 0.270), and there was no interaction between hypertension and chronic exposure to angiotensin II or captopril (P = 0.950). We conclude that renal degradation of angiotensin II is constitutively high, is unaffected by chronic levels of arterial blood pressure, and is independent of long-term changes in levels of angiotensin II.