奈比洛尔对自发性高血压大鼠循环和主动脉肾素-血管紧张素系统的影响

目的：探讨奈比洛尔（Nebivolol）对自发性高血压大鼠循环和主动脉肾素-血管紧张素系统（RAS）的影响。方法：18只自发性高血压大鼠（SHR）和6只同源正常血压大鼠Wistar-Kyoto（WKY）随机分为：（1）奈比洛尔组（n=6）：SHR给予奈比洛尔5mg·kg-1·d-1;（2）卡托普利组（n=6）：SHR给予卡托普利15mg·kg-1·d-1;（3）SHR对照组（n=6）;（4）WKY对照组（n=6）。奈比洛尔、卡托普利溶于蒸馏水中灌胃,对照组给予等体积蒸馏水灌胃。给药8周后测定血浆肾素活性（PRA）,血浆和主动脉血管紧张素Ⅱ（AngⅡ）、一氧化氮（NO）浓度,NO/AngⅡ和血管紧张素转化酶（ACE）活性。结果：与WKY比较,SHR血浆和主动脉NO含量降低,AngⅡ水平显著增加,NO/AngⅡ降低;主动脉ACE活性明显增加,而血浆ACE活性则降低;但PRA在两组间无显著性差异。奈比洛尔治疗对SHR血浆AngⅡ含量和ACE活性无影响,但可降低主动脉AngⅡ水平,抑制主动脉ACE活性,从而增加血浆及主动脉NO含量和NO/AngⅡ。结论：奈比洛尔抑制肾素-血管紧张素系统,可能是其降低血压的机制之一。     

血管紧张素-(1-7)对肾性高血压大鼠血压的影响

目的：探讨急性血管紧张素-（1-7）[Ang-（1-7）]对二肾一夹（2K1C）高血压大鼠血压的作用及其机制。方法：建立2K1C高血压大鼠模型后2周,经颈内静脉输注Ang-（1-7）,同时多导电生理仪记录有创颈动脉压演变。放免法测定血浆AngⅡ,酶法测定血清一氧化氮（NO）,酶免疫法测定血浆前列腺素E2（PGE2）、精氨酸加压素（AVP）,ELISA法测定血浆去甲肾上腺素（NE）。结果：Ang-（1-7）造成2K1C大鼠血压先升高,而后又降低到基础水平之下并维持该水平。与低血压状态相伴随,血清NO及血浆PGE2浓度升高（P〈0.01）,血浆NE及AVP浓度降低（P〈0.05）,血浆AngⅡ水平无明显变化。结论：在高肾素-血管紧张素系统活性状态下,Ang-（1-7）有降压作用,其降压机制与循环NO、PGE2浓度升高及AVP、NE水平降低有关。     

米非司酮对胰岛素抵抗高血压大鼠血管收缩功能的影响

目的：考察米非司酮对胰岛素抵抗高血压大鼠血管收缩功能的影响。方法：将40只雄性sD大鼠随机分为正常组、模型组、罗格列酮（O．4mg·kg-1）组、米非司酮低剂量（20mg·kg-1）组、米非司酮高剂量（40mg·kg-1）组。除正常组外均予以高脂饮食饲养,8周后,取血样测定各组大鼠空腹胰岛素含量、空腹血糖含量,并计算胰岛素敏感指数及抵抗指数以判断胰岛素抵抗模型是否形成,测定血清皮质酮浓度以考察胰岛素抵抗形成过程中糖皮质激素的变化,测定。肾上腺素和去甲肾上腺素浓度以考察交感神经紧张程度,并于实验期间采用套尾法每4周测定1次血压。实验8周末处死大鼠,取出胸主动脉,制备胸主动脉环。用氯化钾预刺激收缩血管环后,分别加入系列浓度的去甲肾上腺素（1X10^-1x10^-5mol·L-1）和血管紧张素Ⅱ（1×10^8、3×10^-8×10^-7、3×10 ^-7和1×10^-6 mol·L-1）,并在地塞米松孵育后再次加入同等系列浓度的去甲肾上腺素。采用生物机能实验系统测定胸主动脉血管的收缩幅度,以氯化钾诱发的最大收缩幅度为100％,将加入去甲肾上腺素或血管紧张素Ⅱ后的血管收缩幅度与氯化钾诱发的最大收缩幅度之间的百分比计为收缩率以反映血管收缩功能。结果：高脂饮食饲养8周可致动物出现高血糖、高胰岛素血症、胰岛素敏感性降低、胰岛素抵抗指数上升,以及血清儿茶酚胺、血清皮质酮水平和血压升高,米非司酮可逆转除皮质酮水平升高以外的上述变化。与正常组相比,模型组大鼠胸主动脉环对去甲肾上腺素及血管紧张素Ⅱ的收缩反应明显增强;与模型组相比,米非司酮高、低剂量组大鼠胸主动脉环对去甲肾上腺素及血管紧张素Ⅱ所致的收缩反应显著降低,用地塞米松孵育后,其对去甲肾上腺素所致的收缩反应与模型组相比无显著变化,但较正常组及未用地塞米松孵育时显著升高。结论：高脂饮食饲养8周可诱导大鼠形成胰岛素抵抗高血压模型并伴有血管收缩功能障碍;米非司酮可改善以上症状,推测其可能通过拮抗糖皮质激素的生物学效应及降低胰岛素抵抗高血压大鼠血管环对血管紧张素Ⅱ的收缩性而发挥作用。     

地龙降压蛋白对自发性高血压大鼠血压及血管紧张素Ⅱ含量的影响

目的初步探讨地龙降压蛋白对自发性高血压大鼠（spontaneously hypertension rat,SHR）的降压作用及对血管紧张素Ⅱ（angiotensinⅡ,AngⅡ）含量的影响。方法应用专利技术从中药地龙中提取地龙降压蛋白,并测定其体外ACE抑制活性。单次静脉注射地龙降压蛋白,颈动脉插管法观察SHR血压的动态变化。选择16周龄SHR32只随机分为SHR模型组、地龙降压蛋白低剂量组、地龙降压蛋白高剂量组、卡托普利组,同时以同源性Wistar大鼠8只作为正常对照组,药物干预28d,用无创尾动脉套袖法测量大鼠血压变化;放射免疫分析法测定大鼠血浆及肾脏局部AngⅡ含量。选择昆明种小鼠60只,以不同剂量腹腔注射给药测定地龙降压蛋白的半数致死量。结果①地龙降压蛋白对ACE的比抑制活力为2.54;②单次及多次给药,地龙降压蛋白均可明显降低SHR血压（P〈0.05）;③药物干预后,与SHR模型组比较,地龙降压蛋白组血浆AngⅡ含量显著降低（P〈0.05）,而肾脏局部AngⅡ虽有所下降,但差异无统计学意义（P〉0.05）;④地龙降压蛋白对昆明小鼠的半数致死量〉20g/kg。结论地龙降压蛋白对SHR有降压作用,其降压机制可能与降低血浆及肾脏局部组织中AngⅡ含量有关。     

地龙降压蛋白对自发性高血压模型大鼠血管紧张素Ⅱ及AT_1受体表达的影响研究

目的:研究地龙降压蛋白对自发性高血压(SHR)模型大鼠的降压作用及对血管紧张素Ⅱ(AngⅡ)、AT1受体表达的影响。方法:单次静脉注射地龙降压蛋白,观察SHR模型大鼠血压的动态变化;地龙降压蛋白连续干预28d,观察对SHR模型大鼠血压变化;同时检测大鼠AngⅡ含量及AT1受体的表达。结果:单次及多次给药,地龙降压蛋白均可显著降低SHR模型大鼠血压(P<0.05);地龙降压蛋白能显著降低SHR模型大鼠血浆AngⅡ水平(P<0.05),而肾脏局部AngⅡ含量虽有所下降,但无显著性差异(P>0.05);与正常对照组比较,SHR模型大鼠肾脏局部AT1受体表达显著增加,经地龙降压蛋白干预,其表达减少。结论:地龙降压蛋白对SHR有降压作用,其降压机制可能与降低AngⅡ含量及抑制肾脏AT受体表达有关。     

镇肝熄风汤对自发性高血压大鼠血管紧张素II、内皮素的影响

目的：观察镇肝熄风汤对自发性高血压大鼠（SHR）的降压效果及其对血浆、心肌、脑组织中血管紧张素Ⅱ（AngⅡ）、内皮素（ET）含量的影响。方法：将24只14周龄的雄性SHR随机分为SHR组、镇肝熄风汤组、依那普利组，同时以同源雄性WKY大鼠8只作为对照组，灌胃给药8周后，用16导生理记录系统记录血压，放射免疫法测血浆、心肌、脑组织中AngⅡ、ET含量。结果：与WKY组相比，SHR组血压升高，且血浆、心肌组织中AngⅡ含量显著升高，脑组织中ET含量升高。镇肝熄风汤可降低SHR血浆及心肌组织中AngⅡ、脑组织中ET含量。结论：镇肝熄风汤可减少缩血管物质（AngⅡ、ET）的释放，对心、脑具有一定的保护作用，可预防高血压并发症。     

肾上腺髓质素前体N端20肽及部分血管活性物质在心衰患者血浆中的变化

为了探讨肾上腺髓质素前体N端20肽（PAMP）在充血性心衰病理生理中的作用,用放免的方法检测22例心衰患者血浆PAMP、内皮素（ET）、血管紧张素Ⅱ（AngⅡ）、去甲肾上腺素（NE）和肾上腺素（E）的浓度,并与正常对照组作比较。结果发现心衰患者血浆PAMP浓度（2884±3．25ng／L）明显高于正常对照组（P＜0．01）,且与ET、AngⅡ、NE和E成正相关（r分别为0．360、0．476、0．475、0．387;P均＜0．05）。提示心衰患者血浆PAMP的升高,可能是机体维持自身稳态的一种代偿机制。     

茶多酚对异丙肾上腺素致大鼠心肌肥厚的保护作用

目的观察茶多酚对大鼠心肌肥厚的保护作用并讨论其相关可能作用机制。方法采用皮下注射异丙肾上腺素（ISO）建立大鼠心肌肥厚模型,将28只SD大鼠随机分为对照组、模型组、美托洛尔组、茶多酚组,灌胃给药连续14d后,取心脏称重后计算全心重量指数及左心重量参数;分别检测测定心肌组织一氧化氮合酶（NOS）活性及心肌组织血管紧张素Ⅱ（AngⅡ）及钙调神经磷酸酶（CaN）的水平。结果与模型组相比,茶多酚能显著改善心脏质量指数,心肌组织NOS活性显著升高、AngⅡ含量降低、CaN活性明显降低。结论茶多酚对异丙肾上腺素所致大鼠心肌肥厚具有保护作用,其作用机制可能与提高NO水平、降低CaN活性、抑制AngⅡ有关。     

香青兰总黄酮对血管紧张素Ⅱ诱导血管平滑肌细胞黏附分子及基质金属蛋白酶表达的影响

目的：研究香青兰总黄酮对血管紧张素Ⅱ（AngⅡ）诱导的大鼠主动脉血管平滑肌细胞（VSMC）黏附分子及基质金属蛋白酶（MMPs）表达的影响。方法：采用贴壁法培养大鼠胸主动脉平滑肌细胞,以AngⅡ为诱导剂,建立VSMC细胞增殖的模型,分别应用10^-7 mol·L^-1AngⅡ以及AngⅡ+不同浓度香青兰总黄酮组（25,50,100 μg·mL^-1）作用24 h,并设空白对照组进行比较。采用免疫组化法检测细胞中细胞间黏附分子（ICAM-1）、血管间黏附分子（VCAM-1）的表达水平。RT-PCR方法检测细胞MMP-2、MMP-9的mRNA表达水平。结果：与对照组比较,AngⅡ组能显著刺激大鼠VSMC细胞内ICAM-1、VCAM-1、MMP-2、MMP-9的表达,香青兰总黄酮不同剂量组联合AngⅡ可在一定程度上抑制AngⅡ诱导的VSMC细胞内ICAM-1、VCAM-1、MMP-2、MMP-9的表达,且呈现一定的剂量依赖关系趋势。结论：香青兰总黄酮具有抑制AngⅡ诱导VSMC黏附分子及基质金属蛋白酶表达的作用。     

纵条矶海葵对高血压大鼠的降压作用

采用监测大鼠颈动脉血压、心电图和呼吸、观察纵条矶海葵提取物对自发性高大鼠及不同因素所致正常大鼠血压变化的影响，以探讨其抗高血压作用。结果显示，纵条矶海葵对正常大鼠及高血压大鼠均有一定的降低血压效应，对心率无明显影响，其降压作用有量效关系，未见有快速耐受现象，不影响肾上腺素、苯肾小腺素、血管紧张素Ⅱ及垂体后叶素对大鼠血压的反应性。提示纵条矾海葵有抗血压作用，且降压时肯反射性增快心率、其降太效应与直接     

PRODUCTION OF EICOSANOIDS AND ANGIOTENSIN II IN RESISTANCE VESSELS IN SPONTANEOUSLY HYPERTENSIVE RATS

1. Angiotensin II (Angll) and eicosanoids may be important in vascular remodelling and the pressor response via autocrine and paracrine mechanisms. We evaluated the influences of ageing and β-adrenoceptor stimulation on the production of vascular Angll and eicosanoids in male spontaneously hypertensive rats (SHR), aged 5,17 and 30 weeks, and age-matched Wistar-Kyoto (WKY) rats. 2. All rats were weighed and their systolic blood pressure (SBP) was measured by the tail-cuff method. Mesenteric arteries were isolated and perfused with Krebs'-Henseleit solution. The outflows of prostaglandin E₂ (PGE₂), 6-keto-PGF_1α, thromboxane B₂ (TxB₂) and AngII were measured by specific radioimmunoassays. 3. The SBP was higher in SHR than in WKY rats in the 17-and 30-week-old groups and increased with age. Basal levels of PGE₂ were significantly lower in SHR than in WKY rats. The ratios of 6-keto-PGF_1α to TxB₂ and PGE₂ to TxB₂ were significantly lower in 17-week-old SHR compared with age-matched WKY rats. Basal Angll release did not differ between SHR and WKY rats and decreased with age. Isoproterenol stimulated the release of Angll; the magnitude of the increment was greater in WKY rats than in age-matched SHR. These results show that there is an imbalance in the production of vasodilator and vasoconstrictor eicosanoids in the resistance vessels of SHR at ages at which hypertension developed. 4. This imbalance may contribute to the increased vasoconstrictor response and vascular remodelling in SHR. Our findings suggest that vascular Angll plays a role in the ageing process and that β-adrenoceptor-stimuIated release of vascular Angll is impaired in SHR.     

Beneficial effects of the combination of nifedipine and losartan in hypertensive Dahl salt-sensitive rats

BACKGROUND: The antihypertensive and organ-protective effects of the combination of the angiotensin II type 1 receptor blocker losartan and the calcium channel blocker nifedipine were examined in Dahl salt-sensitive rats. METHODS: The rats fed with a high-salt diet developed hypertension accompanied by aorta and heart hypertrophy, and impaired renal function. The animals were treated with losartan (30 mg/kg/day), nifedipine (7.8 mg/kg/day) or with a combination of both drugs for 8 weeks. At the end of the study systolic blood pressure, kidney function, organ weight, and mRNA expression were investigated. RESULTS: Losartan reduced significantly the systolic blood pressure as well as the aorta and left ventricular hypertrophy. Nifedipine and its combination with losartan had similar effects on the systolic blood pressure, aorta and left ventricular hypertrophy but only the combination treatment reduced the expression of transforming growth factor-beta1 in aorta and brain natriuretic peptide in left ventricle significantly. Nifedipine and the combination therapy reduced proteinuria and improved urine creatinine excretion. The expression of collagen III and IV in the kidney was significantly reduced by the combination therapy. CONCLUSION: These results indicate that although losartan and nifedipine were effective in lowering blood pressure and showed moderate organ protection, additional benefits can be expected by combination therapy with both compounds.     

长期雾化吸入硝酸甘油对高肺血流量大鼠肺动脉压力影响的研究

目的　探讨长期雾化吸入硝酸甘油对高肺血流量所致大鼠肺动脉高压的作用。方法　 2 4只健康♂Wistar大鼠随机分为对照组 (n =11)、分流组 (n =6 )和吸入组 (n =7)。对分流组和吸入组大鼠开腹行腹主动脉 下腔静脉分流术。12wk后分流组和吸入组大鼠分别雾化吸入生理盐水和硝酸甘油 3wk。以右心导管测定肺动脉压 (pulmonaryarterialpres sure ,PAP) ,颈动脉插管测定体循环压 (systemicarterialpres sure ,SAP)。检测右心室 /体重 (RV/BW)和右心室 /左心室 +室间隔 [RV/ (LV +S) ]比值 ,并且观测肺血管结构变化。结果　分流组大鼠肺动脉收缩压 (PASP)、RV/BW和RV/ (LV +S)明显高于对照组 (P <0 0 1) ,且分流组大鼠肺小血管肌化程度明显增强 (P <0 0 1)。吸入组大鼠SAP未受影响 ,PASP及PAMP明显低于分流组 (P <0 0 1) ,RV/BW和RV/ (LV +S)高于对照组 (P <0 0 1) ,但与分流组比较无差异 (P >0 0 1) ,吸入组大鼠肺小血管肌型动脉与分流组比较明显减少 ,肌化程度明显降低。结论　长期雾化吸入硝酸甘油可缓解高肺血流量所致肺动脉高压和肺血管结构重建     

左前肢血压法动态观察腹主动脉缩窄大鼠的血压变化

目的考察左前肢血压法可否应用于动态观察腹主动脉缩窄大鼠的血压变化。方法腹主动脉缩窄法建立♂SD大鼠压力负荷心肌肥厚模型,实验动物分为假手术组和腹主动脉缩窄/模型组。改进尾动脉血压测量分析系统的尾巴固定装置。采用尾动脉血压法和左前肢血压法测定模型组大鼠和假手术组大鼠的尾动脉压和左前肢动脉收缩压。应用颈动脉插管法测定大鼠在体血流动力学指标,随后测定形态测量学指标。结果与尾动脉血压法比较,左前肢血压法所得血压数据稳定可靠。假手术组大鼠的尾动脉压和左前肢动脉血压值无明显差异。与假手术组动物相比,术后模型组大鼠左前肢收缩压明显上升。术后24wk颈动脉收缩压和舒张压明显升高;心脏重量指数和左室心重指数明显升高。左前肢动脉压与颈动脉收缩压呈线性正相关。结论与尾动脉血压法相比,左前肢血压法可克服腹主动脉缩窄大鼠动态血压观察的困难,其方法可靠且可行,尤其适用于动态观察腹主动脉缩窄程度严重大鼠的血压变化。     

丁咯地尔对大鼠外周离体血管的药理作用

目的 :分析丁咯地尔对大鼠外周血管的药理作用及机制。方法 :采用离体血管平滑肌张力实验 ,研究其对多种因素引起大鼠尾动脉、胸主动脉收缩作用的影响。结果 :丁咯地尔可浓度依赖性地使去甲肾上腺素、去氧肾上腺素、可乐定和 5 羟色胺引起的大鼠尾动脉收缩的累积对数浓度 反应曲线平行右移 ,最大反应不降低 ,其pA2 分别为 5.4 5,7.2 5,5.97和 6.58。使去甲肾上腺素致大鼠胸主动脉 ;氯化钾、氯化钙致大鼠尾动脉、胸主动脉收缩的累积对数浓度 反应曲线右移 ,最大反应降低 ,其pD′2 分别为 3.88,3.76,3.33,4 .0 3和 3.60。结论 :丁咯地尔可竞争性拮抗大鼠尾动脉的肾上腺素α受体(α1,α2 受体 )和 5 羟色胺受体 ,还可非竞争性拮抗氯化钾、氯化钙致大鼠尾动脉、胸主动脉的收缩     

新型类肽化合物iQWcF对内皮素受体功能的拮抗作用

目的　评价新型类肽化合物iQWcF对内皮素受体功能的拮抗作用。方法　①在大鼠离体主动脉血管条上 ,先以一定浓度的iQWcF孵育 ,然后累积给予不同浓度的ET 1,以ET 1诱发的血管收缩为指标评价iQWcF对ET受体的拮抗特点。②采用麻醉正常血压大鼠 ,预先静脉给予一定剂量的iQWcF。 5min后静脉注射ET 1(0 9nmol·kg-1) ,观察不同时间点血压的变化 ,以评价iQWcF对ET受体的作用。结果　①化合物iQWcF能浓度依赖地抑制ET 1诱发的大鼠主动脉血管条的收缩。②iQWcF静脉注射 30mg·kg-1能抑制ET 1诱发的升压作用。而对ET 1诱发的降压作用无影响。结论　新结构化合物iQWcF是一选择性的ETA 受体拮抗剂     

Antihypertensive effect of 5-HT1A agonist buspirone and 5-HT2B antagonists in experimentally induced hypertension in rats

We investigated the antihypertensive effect of 5-HT1A agonist (buspirone) and 5-HT2B antagonists (SB204741 and SB200646) in deoxycorticosterone acetate (DOCA)-salt-induced hypertensive rats. Experiments were divided into two sets: in the first set, sham-operated control and DOCA-treated hypertensive rats received buspirone (1 mg/kg/day p.o. for 4 weeks) and in the second set, in vivo and in vitro studies were carried out. In the case of in vivo studies, sham-operated control and DOCA-treated hypertensive rats received SB204741 or SB200646 (1 mg/kg/week i.v. for 4 weeks). Blood pressure was measured weekly by tail-cuff method. After completion of the treatment schedule, blood pressure and vascular reactivity to various agonists like 5-HT, noradrenaline and adrenaline were recorded. Chronic administration of buspirone, SB204741 and SB200646 produced a significant reduction in blood pressure and vascular reactivity to agonists in DOCA-salt hypertensive rats, implying an antihypertensive effect. However, chronic administration of the same drugs in sham control rats did not alter blood pressure and vascular reactivity to various agonists. For in vitro studies a similar treatment schedule was followed as in vivo studies and a cumulative concentration response curve of 5-HT was recorded on isolated thoracic aorta. Treatment with 5-HT2B antagonists shifted the concentration response curve of 5-HT to the right on isolated aorta. We conclude that 5-HT1A agonist and 5-HT2B antagonists possess an antihypertensive effect.     

The change of beta-adrenergic system in lead-induced hypertension

Lead exposure is considered to be a risk factor of cardiovascular disease. To investigate the relationship between lead and cardiovascular disease/hypertension in lead exposure, beta-adrenergic system is explored in this study. We address three topics in this study: (a) the relationship between beta-adrenergic receptor and lead level in heart, aorta, and kidney of lead-exposed rats; (b) the relationship between beta-adrenergic receptor in heart, aorta, kidney, and blood pressure in lead-exposed rats; and (c) the change of cyclic AMP level in heart, aorta, and kidney of rats with different lead levels. Wistar rats were chronically fed with 2, 1, 0. 5, 0.1, 0.05, and 0.01% lead acetate and water for 2 months. Plasma catecholamine level was measured by high-performance liquid chromatography. Radioligand binding assay was measured by a method that fulfilled strict criteria of beta-adrenoceptor using the ligand [(125)I]iodocyanopindolol. Cyclic AMP (cAMP) level was determined by radioimmunoassay. The levels of lead were determined by electrothermal atomic absorption spectrometry. The results showed that increased plasma norepinephrine level, decreased aorta beta-adrenergic receptor and cAMP, and increased kidney beta-adrenergic receptor and cAMP contributed to the elevation of blood pressure in lead-induced hypertension. The decrement of beta-adrenoceptor and cAMP in heart resulted in decreased contractility in heart.     

坎地沙坦对盐负荷高血压大鼠主动脉氧化应激-低密度脂蛋白受体-1通路的抑制

目的探讨血管紧张素Ⅱ(AngⅡ)受体拮抗剂坎地沙坦对盐负荷易卒中自发性高血压大鼠(SHRSP)主动脉氧化应激-低密度脂蛋白受体-1通路的影响。方法12wk龄Wistar-Kyoto(WKY)大鼠和SHRSP予8%高盐饮食。高盐WKY大鼠(WKY,n=6)作为对照组,高盐SHRSP随机分为3组:①坎地沙坦组(Can,n=6),予坎地沙坦1·0mg·kg-1·d-1灌胃;②三氯噻嗪组(TCM,n=6),予TCM1·6mg·kg-1·d-1;③SHRSP组(SHRSP,n=6),予等量溶媒。用尾部袖套测量法每周检测1次血压。大鼠给药2wk后摘取胸主动脉,留取24h尿量。采用实时定量PCR检测胸主动脉NAD(P)H氧化酶亚单位p22 phox、p47 phox和gp91 phox mRNA表达,RT-PCR方法检测氧化型低密度脂蛋白受体-1(LOX-1)和Ⅳ型胶原mRNA表达,免疫组化检测血管gp91 phox和LOX-1蛋白表达,ELISA方法检测尿白蛋白排泄。结果实验2wk末,SHRSP组收缩压高于WKY组,坎地沙坦和TCM均降低了高盐SHRSP收缩压(P<0·01),但二者降压幅度无差别(P>0·05)。p47 phox、gp91 phox和LOX-1 mRNA在主动脉中的表达,SHRSP组高于WKY组,坎地沙坦下调了高盐SHRSP p22 phox、gp91 phox和LOX-1 mRNA的表达(P<0·01),抑制了主动脉Ⅳ型胶原mRNA的表达(P<0·01),降低了尿微量白蛋白水平。主动脉免疫组化,WKY组几乎不表达gp91 phox和LOX-1,SHRSP组表达明显增强,坎地沙坦下调了高盐SHRSP主动脉gp91 phox和LOX-1的表达。等效降压剂量的TCM对高盐SHRSP主动脉NAD(P)H氧化酶亚单位、LOX-1、Ⅳ型胶原的表达和尿微量白蛋白水平无明显影响。结论坎地沙坦减轻了盐负荷SHRSP血管损伤,其机制可能与抑制氧化应激LOX-1通路有关,而不一定依赖其降压作用。