黄芪及缬沙坦对肾型高血压大鼠心脏血管紧张素转化酶2表达的影响

目的:探讨两肾一夹高血压大鼠心脏血管紧张素转化酶2(Angiotensin-Converting Enzyme2,ACE2)mRNA、蛋白表达水平及甘肃定西黄芪(Astragalus in Gansu Dingxi,Ast)和缬沙坦(Valsartan,Val)对其表达的影响。方法:健康雄性Wistar大鼠,体重180~200g,构建两肾一夹KIC高血压模型。术后随机分为5组,假手术组;②2KIC组;③Val+2KIC组;④Ast+2KIC组(低剂量);⑤Ast+2KIC组(高剂量)。在观察期末,分别测定各组大鼠体重、心脏湿重,计算出心脏重量/体重;光镜下观察心肌结构的变化;RT-PCR检测各组心肌组织ACE2mRNA,免疫组化测定其蛋白表达。结果:与假手术组比较,2KIC组、Val+2KIC、Ast+2KIC组(低剂量)、Ast+2KIC组(高剂量)心脏重量/体重均升高(P<0.05);②与假手术组比较,2KIC组ACE2mRNA、蛋白表达显著减少;与2KIC组比较,Val+2KIC组及Ast+2KIC组(高剂量)经8周治疗后,ACE2mRNA、蛋白表达量增加(P<0.05)。结论:高血压大鼠心脏ACE2m...     

苯那普利、缬沙坦对自发性高血压大鼠肾脏血管紧张素转换酶2表达的影响

目的观察苯那普利与缬沙坦对自发性高血压大鼠(SHR)血浆血管紧张素Ⅱ(AngⅡ)和肾脏血管紧张素转换酶2(ACE2)表达水平的影响,探讨ACE2在高血压发病机制和药物治疗中的意义。方法12周龄雄性SHR28只,分为空白对照组(Sc)、苯那普利组(10mg/kg.d)(Sb)、小剂量缬沙坦组(10mg/kg.d)(Sl)、大剂量缬沙坦组(30mg/kg.d)(Sh),每组7只,7只雄性WKY大鼠为正常对照。药物治疗3月后,用放射免疫法测定血浆AngⅡ含量,RT-PCR法测定肾脏中ACE和ACE2mRNA的表达水平,免疫组化法比较肾脏中ACE2蛋白的表达。结果与WKY大鼠相比,SHR肾脏中ACE2mRNA及其蛋白的表达均明显降低,而ACEmRNA的表达和血浆AngⅡ水平则明显升高(P<0.05)。缬沙坦治疗后SHR血压显著下降而血浆AngⅡ水平则进一步升高,肾脏中ACE2的表达水平明显升高,且呈剂量依赖性(P<0.05)。苯那普利治疗对SHR血浆AngⅡ水平及肾脏ACE2的表达则无明显影响。结论SHR体内ACE和ACE2的表达失衡可能在高血压的发病机制中有重要意义。血管紧张素受体拮抗剂(ARB)可能通过升高SHR血浆AngⅡ的水平而增加肾脏中ACE2的表达,ACE2表达的增加可能是ARB抗高血压治疗的一个新药理机制。     

自发性高血压大鼠肾脏血管紧张素转换酶2 mRNA转录及其蛋白表达

目的 观察不同月龄自发性高血压大鼠(SHR)肾脏血管紧张素转换酶2(ACE2)mRNA转录及其蛋白表达,初步探讨ACE2在高血压发生、发展过程中的可能作用.方法 雄性SHR 1月龄组(S1)、2月龄组(S2)、3月龄组(S3)、6月龄组(S6)和9月龄组(S9)共5组,每组各6只,各组均有相应月龄匹配的Wistar-Kyoto(WKY)大鼠作对照.采用RBP-Ⅰ型大鼠血压心率测定仪测量大鼠尾动脉收缩压(SBP);逆转录聚合酶链式反应(RT-PCR)法检测肾脏ACE2 mRNA的转录水平;免疫组化染色结合计算机图像分析方法 测定肾脏ACE2蛋白的表达水平.结果 1)SHR的SBP随着月龄的增加而上升,6月龄后趋于稳定.2)SHR和WKY肾脏ACE2蛋白和mRNA水平均随着月份的增加而增加,3月龄时达高峰,6月龄后趋于稳定;且SHR肾脏ACE2蛋白和mRNA水平均低于同龄的WKY.S1肾脏髓质内侧部ACE2免疫染色阳性面积百分比较皮质和髓质外侧部高,与1月后的分布相反.结论 1)SHR肾脏ACE2 mRNA和蛋白的表达水平比WKY大鼠低.2)大鼠肾脏ACE2 mRNA和蛋白的表达具有时间和部位分布上的差异.     

苯那普利、缬沙坦对自发性高血压大鼠肾脏血管紧张素转换酶2表达的影响

目的观察苯那普利与缬沙坦对自发性高血压大鼠(SHR)血浆血管紧张素Ⅱ(Ang Ⅱ)和肾脏血管紧张素转换酶2(ACE2)表达水平的影响,探讨ACE2在高血压发病机制和药物治疗中的意义.方法12周龄雄性SHR 28只,分为空白对照组(Sc)、苯那普利组(10 mg/kg·d)(Sb)、小剂量缬沙坦组(10 mg/kg·d)(Sl)、大剂量缬沙坦组(30 mg/kg·d)(Sh),每组7只,7只雄性WKY大鼠为正常对照.药物治疗3月后,用放射免疫法测定血浆Ang Ⅱ含量,RT-PCR法测定肾脏中ACE和ACE2 mRNA的表达水平,免疫组化法比较肾脏中ACE2蛋白的表达.结果与WKY大鼠相比,SHR肾脏中ACE2 mRNA及其蛋白的表达均明显降低,而ACE mRNA的表达和血浆Ang Ⅱ水平则明显升高(P<0.05).缬沙坦治疗后SHR血压显著下降而血浆Ang Ⅱ水平则进一步升高,肾脏中ACE2的表达水平明显升高,且呈剂量依赖性(P<0.05).苯那普利治疗对SHR血浆Ang Ⅱ水平及肾脏ACE2的表达则无明显影响.结论SHR体内ACE和ACE2的表达失衡可能在高血压的发病机制中有重要意义.血管紧张素受体拮抗剂(ARB)可能通过升高SHR血浆Ang Ⅱ的水平而增加肾脏中ACE2的表达,ACE2表达的增加可能是ARB抗高血压治疗的一个新药理机制.     

自发性高血压大鼠肾脏血管紧张素转换酶2 mRNA转录及其蛋白表达

目的观察不同月龄自发性高血压大鼠(SHR)肾脏血管紧张素转换酶2(ACE2) mRNA转录及其蛋白表达,初步探讨ACE2在高血压发生、发展过程中的可能作用。方法雄性SHR1月龄组(S1)、2月龄组(S2)、3月龄组(S3)、6月龄组(S6)和9月龄组(S9)共5组,每组各6只,各组均有相应月龄匹配的Wistar-Kyoto(WKY)大鼠作对照。采用RBP-Ⅰ型大鼠血压心率测定仪测量大鼠尾动脉收缩压(SBP);逆转录聚合酶链式反应(RT-PCR)法检测肾脏ACE2 mRNA的转录水平;免疫组化染色结合计算机图像分析方法测定肾脏ACE2蛋白的表达水平。结果1)SHR的SBP随着月龄的增加而上升,6月龄后趋于稳定。2)SHR和WKY肾脏ACE2蛋白和 mRNA水平均随着月份的增加而增加,3月龄时达高峰,6月龄后趋于稳定;且SHR肾脏ACE2蛋白和 mRNA水平均低于同龄的WKY。S1肾脏髓质内侧部ACE2免疫染色阳性面积百分比较皮质和髓质外侧部高,与1月后的分布相反。结论1)SHR肾脏ACE2 mRNA和蛋白的表达水平比WKY大鼠低。2)大鼠肾脏ACE2 mRNA和蛋白的表达具有时间和部位分布上的差异。     

缬沙坦对自发性高血压大鼠组织内肾素-血管紧张素的影响

目的     

自发性高血压大鼠心脏重构与ACE2 mRNA的表达

目的:观察不同月龄的自发性高血压大鼠(SHR)的心脏血管紧张素转换酶2(ACE2)mRNA表达水平,探讨心脏重构与ACE2的内在联系。方法:将12周龄雄性SHR 18只和12周龄WKY Wistar-Kyoto rats大鼠18只随机分为两组,从WKY大鼠组和SHR组中各抽取9只处死,剩余的9只再喂养12周后处死。测量大鼠心脏的质量(HW)与体质量(BW)并计算HW/BW的比值。以实时定量RT-PCR法检测ACE2 mRNA的表达。结果:①与同周龄WKY大鼠组比较,SHR组HW/BW的比值显著增加(P0.01);与12周龄SHR组比较,24周龄SHR组的HW/BW显著增加(P0.05)。②与同周龄的WKY大鼠组比较,SHR组ACE2 mRNA的表达显著降低(P0.01);与12周龄的SHR组比较,24周龄的SHR组ACE2 mRNA的表达显著降低(P0.01)。结论:自发性高血压大鼠心脏重构伴随着心脏中ACE2 mRNA的表达下调。     

血管紧张素转化酶2基因多态性与原发性高血压的关系

目的研究血管紧张素转化酶2基因（ACE2-G8790A）单核苷酸多态性（SNP）与原发性高血压的关系。方法用PCR—RFLP及电泳分析法进行基因分型,SPSS软件分析各等位基因与原发性高血压的相关性。结果高血压患者与对照组的基因型、等位基因频率比较均有显著性差异（P=0．020,0．001）。高血压组GG、GA和AA基因型在女性中的分布频率分别为29．2％、42．4％和28．4％,女性对照组相应基因型的频率分别为29．3％、56．6％和14．1％,两组比较有显著性差异;G,A等位基因频率在高血压组分别为53．0％和47．0％,对照组相应的等位基因频率为63．3％,36．7％,两组比较差异有显著性（P〈0．01）。结论ACE2-G8790A基因多态性与原发性高血压相关。     

氢氯噻嗪对不同血管紧张素转化酶基因型高血压患者血浆血管紧张素转化酶血管紧张素Ⅱ浓度的影响

目的研究氢氯噻嗪(HCTZ)对不同血管紧张素转化酶(ACE)基因型的原发性高血压患者血浆ACE浓度和血管紧张素Ⅱ(AngⅡ)浓度的影响。方法829例原发性高血压患者同时服用HCTZ12.5mg,qd。6周后资料完整的785例患者按II、ID、DD3种基因型分组,观测不同基因型间血浆ACE浓度、AngⅡ浓度的变化。结果服用HCTZ6周后II、ID、DD型患者血浆ACE浓度较服药前稍增高,但差异无统计学意义;血浆AngⅡ浓度分别升高到(85.56±64.68)、(81.97±57.99)和(80.84±67.96)ng/L,与服药前比较均差异有统计学意义。3组不同基因型患者血浆AngⅡ服药前后组间差异无统计学意义。结论服HCTZ后,3组基因型患者血浆AngⅡ浓度均升高,血浆ACE浓度不是影响血浆AngⅡ浓度的主要因素。     

缬沙坦对自发性高血压大鼠血管紧张素ⅡⅠ型受体密度及亲和力干预的研究

目的研究缬沙坦对自发性高血压大鼠左室心肌血管紧张素ⅡⅠ型受体(AT1)密度及亲和力的影响,探讨高血压左室肥厚的细胞分子机制及缬沙坦的干预机制.方法 (1)12只6周龄雄性自发性高血压大鼠(SHR)分二组自发性高血压大鼠(SHR)6只为阳性对照组;缬沙坦干预组(SHR-V)6只 缬沙坦 20 mg*kg-1*d-1;同源正常血压大鼠(WKY)6只为正常对照组.(2)用放射配基结合分析法测定左室心肌AT1受体密度及亲和力;用放免法测定血液及左室心肌血管紧张素Ⅱ(Ang Ⅱ)浓度;测量血压、左室重量/体重及左室厚度/体重.结果 (1)AT1受体密度及亲和力的变化SHR组左室心肌AT1受体亲和力较WKY组增强(P<0.05),但AT1受体密度降低(P<0.01);SHR-V组较SHR组AT1受体亲和力降低(P<0.05),与WKY组无明显的差异,在SHR-V组,AT1受体密度明显高于SHR组(P<0.01).(2)Ang Ⅱ浓度的变化SHR组心肌Ang Ⅱ水平较WKY组明显升高(P<0.01),但血浆Ang Ⅱ水平无明显差异;SHR-V组心肌Ang Ⅱ水平明显低于SHR组(P<0.01),而血浆Ang Ⅱ浓度较另二组明显升高(P<0.01).(3)血压及左室结构的变化缬沙坦可显著降低SHR的血压、左室重量/体重及左室厚度/体重(P<0.01).结论 (1)左室心肌AT1受体亲和力增强及Ang Ⅱ水平升高在高血压左室肥厚的发生、发展中起着重要的作用.(2)缬沙坦除可降低血压外,尚可降低左室心肌AT1受体亲和力及Ang Ⅱ水平,逆转左室肥厚.     

ACE2和ACE在自发性高血压大鼠心肌中的变化

目的:观察自发性高血压大鼠(SHR)心肌的血管紧张素转化酶(ACE)和ACE2的表达,以探讨ACE2和ACE在高血压发生发展中的变化。方法:取15只SHR,处死,分离左心室,行RT-PCR、Western blot蛋白质免疫印迹和免疫组织化学检测ACE及ACE2表达;同步取10只WKY大鼠作为正常血压对照组。结果:SHR组心肌ACE的mRNA和蛋白质表达都显著高于WKY组[(1.68±0.34)∶(0.33±0.12),P<0.05;(1.21±0.14)∶(0.71±0.11),P<0.05],而ACE2的mRNA和蛋白质表达皆明显低于WKY组[(0.50±0.15)∶(1.16±0.24),P<0.05;(0.71±0.24)∶(1.22±0.14),P<0.05)]。免疫组织化学染色显示,SHR组ACE的阳性率明显高于WKY组(87%∶50%,P<0.05),而ACE2的阳性率明显低于WKY组(27%∶70%,P<0.05)。结论:SHR心肌ACE明显升高,ACE2显著降低;SHR高血压发生发展过程中存在着ACE和ACE2表达的失衡。     

大豆低聚肽对自发性高血压大鼠降血压作用的研究

目的探讨不同剂量的大豆低聚肽(SBOP)对自发性高血压大鼠(SHR)的降血压作用及其机制.方法6～8周龄雌性SHR大鼠30只及同周龄同体重Sprague-Dawley(SD)雌性大鼠6只随机分为A组(SHR对照组,饮水中不加SBOP及药物卡托普利)、B组[SBOP低剂量组,饮水中按100 mg/(L·d)加入SBOP]、C组[SBOP中剂量组,饮水中按500 mg/(L·d)加入SBOP]、D组[SBOP高剂量组,饮水中按1000 mg/(L·d)加入SBOP]、E组[卡托普利药物处理组,饮水中按50 mg/(L·d)加入卡托普利],F组[SD正常血压对照组,饮水中按1000 mg/(L·d)加入SBOP],实验期共30 d.尾袖法测定大鼠尾动脉血压,比色法测定血清及组织血管紧张素转换酶(angiotensin converting enzyme,ACE)活性.结果给予低、中、高3种剂量的SBOP 30 d后SHR大鼠血压分别为(155.5±15.6),(153.0±4.5),(151.5±5.0)mmHg,卡托普利药物处理组为(148.0±15.6)mmHg,SHR对照组为(174.0±11.5)mmHg,正常SD大鼠为(136.5±9.6)mmHg(P＜0.05).SBOP组与SHR对照组血清及主动脉ACE活性分别为(0.0118±0.069),(0.0121±0.0011),(0.0305±0.0048),(0.0290±0.0037)U(P＞0.05),而卡托普利药物处理组为(0.0054±0.0016),(0.0219±0.0039)U(P＜0.05).血清钠离子浓度SBOP、卡托普利药物处理组分别为(0.0896±0.0050),(0.0900±0.0012)μmol/L,SHR对照组为(0.1028±0.0056)μmol/L(P＜0.05).结论中、高剂量SBOP能有效地降低SHR大鼠的血压,且随剂量的增加血压有呈指数下降的趋势,但SBOP的降压效果始终不及降压药物卡托普利.SBOP对正常血压大鼠的血压无影响.SBOP降血压作用可能与降低外周组织液钠离子浓度有关,而与降低ACE活性无关.     

Trimethylamine-N-oxide (TMAO) increased aquaporin-2 expression in spontaneously hypertensive rats

Recent evidence suggests that elevated plasma levels of Trimethylamine-N-oxide (TMAO) can prolong the duration of elevated blood pressure in rats. The purpose of this study was to investigate the plasma TMAO level in Spontaneously Hypertensive Rats (SHR) and to explore the possible relationship between TMAO and aquaporin-2 (AQP-2) in the formation of hypertension. Twelve-week-old, male Spontaneously Hypertensive rats (SHR, n = 40) and Wistar-Kyoto rats (WKY, n = 40) were accordingly grouped into SHR group and WKY group. Each group was divided randomly into four subgroups: Untreated group, TMAO group, TMAO+Tolvaptan (TMAO+TVP) group, and TVP group, respectively. Systolic blood pressure (SBP), plasma TMAO, plasma osmolality (POsm), plasma vasopressin (PAVP), and plasma AQP-2 (PAQP-2) concentration were measured, and the expression of AQP-2 in kidney medulla was detected by RT-PCR and Western blot. At 14 weeks, rats in SHR TMAO group were shown the increased plasma TMAO, POsm, PAVP, and PAQP-2 levels, while those rats in SHR TMAO+TVP group were shown the decreased plasma TMAO, POsm, and PAQP-2 levels, but an even higher PAVP (due to the blockage of TVP to V2 receptor). These findings indicate that an increase of plasma TMAO levels in SHR leads to a higher plasma osmotic pressure, triggers the regulation of the TMAO-AVP-AQP-2 axis in SHR, elicits the greater water reabsorption, and eventually leads to hypertension.     

培哚普利对肾性高血压大鼠肾脏血管紧张素转换酶2的影响

目的采用两肾一夹(2K1C)高血压大鼠模型,了解培哚普利对高血压大鼠肾脏血管紧张素转换酶2(ACE2)表达的影响。方法40只雄性大鼠随机分为5组:正常对照组;2K1C高血压组;缬沙坦组;高剂量培哚普利组;低剂量培哚普利组。给药8周后,计算心重指数,放射免疫分析法测定血浆血管紧张素(Ang)Ⅱ水平,逆转录聚合酶链反应(RT-PCR)检测肾脏ACE2 mRNA表达,免疫组织化学法检测肾脏ACE2表达。结果培哚普利和缬沙坦治疗都明显降低高血压大鼠血压(P<0.01);RT-PCR和免疫组织化学染色结果显示2K1C高血压大鼠肾脏ACE2表达较正常大鼠降低(P<0.05);经培哚普利及缬沙坦治疗后大鼠ACE2表达明显高于2K1C高血压组(P<0.05)。高剂量培哚普利组血浆AngⅡ降低较缬沙坦组明显(P<0.01)。2K1C高血压大鼠心重指数明显高于各给药组(P<0.01)。结论2K1C高血压大鼠肾脏组织中ACE2表达降低,培哚普利及缬沙坦在降压的同时能增加肾脏组织ACE2的表达。     

地龙降压胶囊对自发性高血压大鼠肾胺酶表达的影响

目的:观察地龙降压胶囊对自发性高血压大鼠(SHR)肾胺酶表达的影响,以探讨地龙降压胶囊治疗原发性高血压的作用机制。方法:取24只8周龄雄性SHR,根据收缩压随机分为模型组(等容量蒸馏水灌胃)及地龙降压胶囊高、低剂量组(分别以地龙降压胶囊240mg/kg、120mg/kg灌胃),每组8只。另取8只WKY雄性大鼠作为正常对照组(等容量蒸馏水灌胃)。分别于连续给药前、给药后第2周、4周、6周、8周测定尾动脉收缩压。末次给药后,采用ELISA法检测大鼠血浆儿茶酚胺和血清肾胺酶含量。采用免疫组织化学法检测大鼠肾脏肾胺酶的表达。结果:地龙降压胶囊有效降低了SHR收缩压、血浆儿茶酚胺水平(P<0.05);升高了SHR肾胺酶水平(P<0.05)。结论:地龙降压胶囊能有效降低血压,其作用机制可能是通过调节肾胺酶表达水平,从而影响血浆儿茶酚胺水平实现的。     

依那普利对自发性高血压大鼠心脏局部血管紧张素转换酶及左室肥厚的作用

目的　研究自发性高血压大鼠 (SHR)心脏局部血管紧张素转换酶 (ACE)活性对左室肥厚的影响及依那普利的作用。方法　选用 1 2w龄SHR 40只 ,随机分为两组 ,一组给予依那普利 30mg/ (kg·d)治疗 ,另一组作为对照 ,同时设一同周龄的WKY作为正常对照 ,用病理学图像分析法检测SHR左心室壁厚度、心肌细胞体积比例 (CVF)和心肌血管周围胶原面积和管腔面积比例 (PVCA) ,放免法测定血管紧张素Ⅱ (AngⅡ )浓度 ,荧光法测定ACE活性。结果　 (1 )SHR治疗组 (SHR T)BW/LV与正常对照组 (WKY C)相比无差异 (P >0 0 5) ;(2 )SHR C组AngⅡ浓度为 (5 780± 3 734)ng/mg组织 ,显著高于WKY C组〔(2 72 3± 0 84)ng/mg组织〕(P <0 0 5) ;而依那普利治疗后SHR T组AngⅡ浓度为 (2 757± 2 71 7)ng/mg组织 ,与WKY C组相比无显著差异。 (3)SHR T、SHR C、WKY C三组ACE活性分别为 (0 47± 0 1 2 )单位 / (ml·mg组织 ) ,(0 60± 0 1 3)单位 / (ml·mg组织 ) ,(0 45± 0 1 9)单位 / (ml·mg组织 ) ,SHR T组与SHR C组比较有显著差异 (P <0 0 1 ) ,SHR T组与WKY C组比较无显著差异 (P >0 0 5)。 (4)SHR T组CVF和PVCA分别为 (1 98± 1 57) %和 (0 68± 0 1 9) % ,显著低于SHR C组〔(5 1 1± 2 2 5) % ,(1 2 0± 0     

mRNA levels of circadian clock components Bmal1 and Per2 alter independently from dosing time-dependent efficacy of combination treatment with valsartan and amlodipine in spontaneously hypertensive rats

Chronopharmacological effects of antihypertensives play a role in the outcome of hypertension therapy. However, studies produce contradictory findings when combination of valsartan plus amlodipine (VA) is applied. Here, we hypothesized different efficacy of morning versus evening dosing of VA in spontaneously hypertensive rats (SHR) and the involvement of circadian clock genes Bmal1 and Per2. We tested the therapy outcome in short-term and also long-term settings. SHRs aged between 8 and 10 weeks were treated with 10 mg/kg of valsartan and 4 mg/kg of amlodipine, either in the morning or in the evening with treatment duration 1 or 6 weeks and compared with parallel placebo groups. After short-term treatment, only morning dosing resulted in significant blood pressure (BP) control (measured by tail-cuff method) when compared to placebo, while after long-term treatment, both dosing groups gained similar superior results in BP control against placebo. However, mRNA levels of Bmal1 and Per2 (measured by RT-PCR) exhibited an independent pattern, with similar alterations in left and right ventricle, kidney as well as in aorta predominantly in groups with evening dosing in both, short-term and also long-term settings. This was accompanied by increased cardiac mRNA expression of plasminogen activator inhibitor-1. In summary, morning dosing proved to be advantageous due to earlier onset of antihypertensive action; however, long-term treatment was demonstrated to be effective regardless of administration time. Our findings also suggest that combination of VA may serve as an independent modulator of circadian clock and might influence disease progression beyond the primary BP lowering effect.     

Inhibition of angiotensin converting enzyme cannot prevent increases in angiotensin II production in coronary circulation

OBJECTIVE—To determine whether inhibition of angiotensin converting enzyme (ACE) can prevent angiotensin II production in the coronary circulation induced by percutaneous transluminal coronary angioplasty (PTCA) in patients with myocardial ischaemia.
DESIGN, PATIENTS—41 patients who underwent elective PTCA and six control subjects who received diagnostic coronary angiography were studied. Patients were divided into two groups according to the chronic administration of ACE inhibitors (group A, 15 patients treated with ACE inhibitors; group B, 26 patients without ACE inhibitors). Blood samples were drawn through catheters placed in the aorta and coronary sinus before and 24 hours after PTCA.
RESULTS—Mean levels of ACE activity in the aorta were significantly lower in patients in group A than in group B. However, mean angiotensin II concentrations in the aorta were not significantly different between the two groups. Differences in basal angiotensin II concentrations between the coronary sinus and aorta, which reflected basal angiotensin II production in the coronary circulation, were not significant among group A, group B, and control subjects. The production of angiotensin II in the coronary circulation was significantly increased 24 hours after PTCA in both group A and group B to the same extent. No significant changes were observed in control subjects 24 hours after diagnostic coronary angiography.
CONCLUSIONS—This study revealed that inhibition of ACE activity by ACE inhibitors could not prevent increases in angiotensin II production in the coronary circulation induced by PTCA.


Keywords: angiotensin converting enzyme; chymase; angioplasty     

The arterial length‐densities under preventive angiotensin‐converting‐enzyme inhibiting treatment in the myocardium of spontaneously hypertensive rats

The length density (L_V) of capillaries is known to be increased in the hearts of spontaneously hypertensive rats (SHR) after high‐dosed but also after low‐dosed subantihypertensive treatment with the ACE‐inhibitor Ramipril administered in utero and post partum. Under the same conditions in the present study only highdose Zabicipril caused an increase of capillary L_V. Under preventive ACE‐inhibition in both high‐dose groups L_V of myocardial arteries was significantly higher. In the low‐dose groups L_V was not significantly increased. The increased arterial L_V in the high‐dose‐group may result from the avoidance of angiotensin II‐induced overabundant growth of myocardial muscle‐mass. Changes in collagen could not be found in any of the experimental groups. (Basic Res Cardiol) Received: 7 April 1997, Returned for 1. revision: 9 June 1997, 1. Revision received: 12 September 1997, Returned for 2. revision: 29 October 1997, 2. Revision received: 31 October 1997, Accepted: 6 November 1997     

新型冠状病毒与血管紧张素转换酶2对心血管系统的影响

自2019年12月起,爆发由新型冠状病毒(SARS-CoV-2)感染的新型冠状病毒肺炎(COVID-19),疫情迅速蔓延至全球。COVID-19以呼吸系统症状为主,但部分病例出现心血管系统损害。合并心血管系统基础疾病患者,会导致死亡率增加。SARS-CoV-2属于冠状病毒科β冠状病毒属,SARS-CoV-2与严重急性呼吸综合征冠状病毒具有79.5%的同源性,通过受体血管紧张素转换酶2(ACE2)入侵人体细胞。而表达ACE2的Ⅱ型肺上皮细胞是SARS-CoV-2感染的主要靶细胞。因此,了解SARS-CoV-2所致心血管系统损害及相关的机制,对SARS-CoV-2疫苗和药物的研制及降低病死率具有重要的意义。