培哚普利与氯沙坦对肾组织一氧化氮浓度及结构的作用比较

目的比较培哚普利和氯沙坦对肾脏的影响，探讨两者对高血压肾的保护机制。方法以高血压鼠非治疗组、培哚普利治疗组、氯沙坦治疗组和正常血压鼠为对象，测量其血压、肾一氧化氮浓度、尿蛋白等指标并观察血管内皮和肾小球结构。结果3月龄高血压鼠电镜下可见血管内皮增生，肾小球基底膜轻度增厚，肾一氧化氮浓度下降、尿蛋白增高，8月龄高血压鼠血管内皮和肾小球均有损害（基底膜增厚、系膜细胞肥大），尿微量白蛋白水平与血管内皮、肾小球病变和肾一氧化氮浓度密切相关，与血压相关性不显著。培哚普利组和氯沙坦组尿微量白蛋白水平较低，且肾一氧化氮浓度较高，血管内皮、系膜细胞的增殖被抑制，培哚普利组一氧化氮水平和尿量显著高于氯沙坦组。结论培哚普利、氯沙坦从多方面保护肾脏，如降压、阻断血管紧张素Ⅱ的增殖效应，提高肾一氧化氮水平、改善肾微循环，减少尿微量白蛋白，且培哚普利对肾一氧化氮的影响显著强于氯沙坦。     

科素亚对高血压鼠肾小球系膜扩张的抑制作用

目的 探讨新一代降压药血管紧张素Ⅱ受体拮抗剂对肾脏(肾小球)的保护作用。方法 由高血压组(SHR)和正常对照血压组(WKY鼠)组成,其中SHR组再分为治疗组[予科素亚20mg/(kg·d)]和非治疗组,分别于三月龄和八月龄测量鼠尾动脉压、及电子显微镜下有关病理指标。结果 与正常血压对照组比较,高血压鼠系膜细胞体密度明显增大,显示增生较前者活跃,可见较多的电子致密物聚积并使整个系膜区体密度扩大。而经科素亚治疗后系膜细胞的过度增生肥大能被有效地抑制,系膜区体密度及细胞外基质较非治疗组明显减少或减少。结论 科素亚在降低动脉压同时,有效地保护了肾脏,抑制高血压肾小球系膜细胞增生及系膜区扩张。     

先兆子痫肾病患者的临床病理及转归

目的:总结19例先兆子痫肾病患者的临床特点、肾活检病理改变特征及转归。方法:19例先兆子痫肾病患者,15例为初产妇,4例为经产妇,平均年龄23～40(28.1±4.5)岁。观察指标包括病程、临床表现、肾功能、尿液检查、肾活检病理、临床与病理联系及临床转归。结果:临床表现为高血压(100%)、蛋白尿(100%),少部分患者伴有镜下血尿(15.8%)和肾功能不全(21.1%)。肾活检组织改变表现为肾小球内皮细胞增生、肿胀(94.7%),系膜细胞增多、系膜基质增加(89.5%),周边袢弥漫或节段双轨(78.9%),肾小球局灶节段硬化(31.6%)。内皮细胞增生指数与终止妊娠时间有关,随着终止妊娠时间的延长,内皮细胞增生、肿胀逐渐消退(P<0.05)。小管间质损害较轻,但是,病理表现为局灶节段性肾小球硬化(FSGS)样损害的患者,小管间质损害较重。血管病变主要表现为小动脉透明变性(36.8%)、内皮肿胀(26.3%)、内膜增厚(26.3%)、弹力层增厚分层(26.3%),严重患者血管壁呈纤维素样坏死(5.3%)。终止妊娠后绝大部分患者,血压下降,尿蛋白减少至转阴,但病理表现FSGS、血管病变较重者尿检异常持续存在。结论:先兆子痫肾病患者临床主要表现为高血压、蛋白尿,部分患者出现镜下血尿,血肌酐升高。肾脏病理特征性表现以内皮细胞病变为主,其他表现包括系膜细胞增多、     

足细胞损伤与糖尿病肾病

糖尿病肾病(diabetic nephropathy,DN)是糖尿病的主要并发症。1936年Kimmelstiel等[1]第一次描述DN时,系膜基质增多和肾小球基底膜(glomerular basement mem-brane,GBM)增厚就被描述为DN的主要病理表现。研究也证实,系膜增生与蛋白尿、肾功能恶化密切相关。但是,系膜增生并不能解释蛋白尿的发生,因为由肾小球内皮细胞、GBM、足细胞构成的肾小球滤过屏障的损伤才是蛋白尿的根源。事实上,肾小球内皮细胞和GBM参与了DN蛋白尿的发生,但两者均是有孔的,均允许某些蛋白通过[2]。因此,足细胞构成了蛋白滤过的最后一道屏障,但其在DN中的生物…     

糖尿病肾病足细胞损伤机制研究进展

糖尿病肾病是终末期肾病的主要病因之一，临床以蛋白尿和肾功能逐渐下降为特点。Kimmelstiel及Wilson首先从组织病理上描述了糖尿病肾病的肾小球系膜基质增加为主要的损伤，而且基底膜增厚曾被认为是重要的病理改变，这些病理改变尤其是系膜基质增生曾认为与蛋白尿形成及肾功能恶化密切相关。然而这些理论并不能完全解释蛋白尿的形成。     

抗血管内皮生长因子药物肾损害合并免疫复合物相关性肾小球肾炎

中年女性患者,确诊肺癌1年半,抗血管内皮生长因子(VEGF)药物治疗后出现水肿,大量蛋白尿和高血压,肾活检组织学为肾小球膜增生性病变伴系膜溶解和内皮细胞病变,同时伴有免疫球蛋白和补体沉积,结合临床,考虑抗VEGF药物肾损害合并免疫复合物相关性肾小球肾炎。     

胰性增生性肾小球肾炎

膜性增生性肾小球肾炎(MPGN)的病理特征是肾小球广泛地受累、小叶增大呈鼓槌状,伴血管系膜细胞增多和血管系膜基质不同程度的硬化,肾小球基底膜(GBM)增厚及分层。临床上可表现为肾病综合征、急性出血性肾炎综合征,也可表现为隐袭性肾衰。经常可见低补体血症,但也可缺乏。本文认为MPGN是一个不同原因引起的病理性损害并且与几个临床病理单位有关。可分为两型。1.伴内皮下沉积物的MPGN:这一型除具有前述共同改变外,可见血管系膜基质或系膜细胞胞浆伸延至其邻近的毛细血管袢,致GBM呈分层表现。电镜见内皮下、分层的GBM间和血管系膜基质内均有沉积物。免疫荧光检查证明     

血管紧张素Ⅱ在糖尿病肾病发病中的作用

血管紧张素Ⅱ在糖尿病肾病发病中的作用胡伟新龚德华综述关键词血管紧张素Ⅱ糖尿病肾病发病机制肾小球、肾小管肥大，基底膜增厚，肾小球高灌注、高压力及微量白蛋白尿是糖尿病肾病（ＤＮ）的早期特征。大量细胞外基质成分在小球系膜区进行性沉积，则导致小球血管袢减少，...     

小鼠肾小球系膜细胞的增龄性改变及油酸对其影响

目的探讨C57BL／6J小鼠肾小球系膜细胞增龄性改变以及油酸对系膜细胞的影响。方法实验动物采用28月龄、3月龄小鼠，测定小鼠血清肿瘤坏死因子α（TNFα）水平，检测系膜细胞的增殖状况，测定肾小球系膜细胞培养上清中胶原Ⅰ、胶原Ⅳ和基质金属蛋白酶2（MMP-2）的含量，观察油酸对系膜细胞的影响。结果28月龄小鼠与3月龄小鼠比较，血清TNFα水平明显增高，分别为（71．6±17．3）μg／L和（59．7±9．7）μg／L，差异有统计学意义（P〈0．05）；肾小球系膜细胞增殖能力明显增强；细胞培养上清中胶原Ⅰ[（52．1±4．6）ng／1万个细胞对（20．3±3．5）ng／1万个细胞]、胶原Ⅳ[（26．3±3．5）ng／1万个细胞对（7．6±1．3）ng／1万个细胞]的水平明显增高；随着鼠龄的增加，细胞培养上清中MMP-2的活性明显下降。油酸可以刺激小鼠肾小球系膜细胞的增殖和胶原Ⅳ的分泌，尤以28月龄小鼠为著。结论与3月龄小鼠比较，28月龄小鼠的肾小球系膜细胞出现明显硬化病变倾向，油酸可刺激28月龄小鼠肾小球系膜细胞的增殖及胶原的分泌。     

警惕生物制剂相关的肾脏损害

正生物制剂,如抗体、酶和激素等,已广泛应用于肿瘤、自身免疫性疾病等。其中单克隆抗体为代表的生物制剂在临床应用已成为治疗疾病的重大突破,而在应用过程中需重视其对肾脏的损害。靶向血管内皮生长因子(VEGF)及其受体(VEGFR)的药物该类药物肾损伤主要表现为高血压和不同程度的蛋白尿。肾损伤病理改变包括内皮增生、小球硬化,透明变性,系膜增生性肾小球肾炎,冷球蛋白血症肾小球肾炎,毛细血管外增生性肾小球肾炎、免疫     

氯沙坦对自发性高血压大鼠阻力血管结构的影响

目的探讨氯沙坦（Losartan）对自发性高血压大鼠（SHR）阻力血管结构的影响,并观察在高血压血管壁增厚的过程中血管紧张素Ⅱ(AngⅡ)所起的作用。 方法采用6周龄雄性SHR20只,随机分为Losartan治疗组（SHRlos）和对照组（SHR）。另选同系雄性6周龄WKY鼠10只作为正常对照组。6周龄SHRlos给予Losartan30mg/kg/d,溶于饮水灌胃治疗17周。颈动脉插管,心电血流动力学监护仪测定动脉收缩压,应用计算机图象分析,计算血管壁腔面积比,用光镜和透射电镜观察SHR肠系膜动脉三级分支结构的变化;血浆放免法测肾素活性和AngⅡ含量。 结果（1）动脉收缩压（SBP）治疗结束后,SHR     

Contractile responses of aortae from WKY and SHR to vasoconstrictors

Aortae taken from spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats aged 4, 8 and 16 weeks were prepared as rings and used to measure the effects of five vasoconstrictors. The endothelium was removed in order to measure selectively the contractile responses induced by potassium chloride (KCl), phenylephrine (PHE), angiotensin-II (Ang II), endothelin-1 (ET-1) and human urotensin-II (U-II). These responses were assumed to derive from the activation of specific receptors (namely alpha1, AT1, ETA and UT-II) or from depolarization of the smooth muscle fibers by KCl. Specific antagonists prazosin, losartan, BQ-123 and [Orn8]-UII were used at various concentrations for a pharmacological characterization of these latter receptor systems. The primary purpose of the study was to explore mechanisms or factors that may intervene in the development and maintenance of high blood pressure in SHR. Results indicate that isolated aortae of SHR and WKY contain contractile sites (receptors) whose pharmacological profiles (pEC50 for agonists, pA2 for antagonists) are very similar to those of other biological systems and should be considered as typical for the alpha1, AT1, ETA and UT-II receptor types. Aortae taken from SHR 4 (non hypertensive), 8 and 16 weeks old (hypertensive) responded to the vasoconstrictors with reduced maximal contractions compared to those of age-matched WKY. These unexpected reduced responses of aortae, observed with the five vasoconstrictors, may be attributed to a non specific lesions. Maximal contraction of aortae from SHR increased from 4 to 16 weeks for KCI, PHE and U-II, decreased for Ang II, and remained stable for ET-1. There was also an age-dependent increase of maximal contraction induced by U-II in WKY. It is suggested that aortae from SHR undergo early remodelling that leads to reduced contractility in vitro and possibly to vessel rigidity in vivo. The factors involved in this process appear to be of genetic origin since they are present before hypertension: they may contribute to modify aortic compliance and perhaps vascular resistance in hypertensive animals and thus being the cause and not the consequence of high blood pressure.     

Blockade of angiotensin II provides additional benefits in hypertension- and ageing-related cardiac and vascular dysfunctions beyond its blood pressure-lowering effects

OBJECTIVES: To assess the blockade of the renin-angiotensin system (RAS) or blood pressure-lowering on cardiovascular functions in hypertensive and ageing animals. METHODS: Male spontaneously hypertensive rats (SHR) and their normotensive counterparts, Wistar-Kyoto rats (WKY), at the ages of 3-4 (young), 34-35 (adult) and 74-75 (old) weeks were treated with an angiotensin II type 1 receptor antagonist, losartan (25 mg/kg) or a combination of a smooth muscle relaxant and a diuretic [H/H, hydralazine (50 mg/kg) plus hydrochlorothiazide (7.5 mg/kg), respectively] for 8 weeks. Each experimental group contained 10 SHR and 10 WKY, where equal numbers of untreated animals served as controls. RESULTS: Compared to age-matched WKY groups, SHR groups possessed, on average, 48 +/- 7 mmHg and 57 +/- 16 mmHg (P < 0.05) higher systolic blood pressure and left ventricular developed pressures, respectively. The values of these parameters were significantly lowered in both strains by both treatment regimens. SHR had higher heart rates, which were increased by H/H treatment selectively in adult and old animal groups of both strains. Both treatment regimens enhanced KCl-mediated, that is, receptor-independent, aortic contractile responses and bradykinin-mediated coronary vasodilatation in adult and old WKY and SHR age-groups. Although both therapies augmented endothelium-dependent and endothelium-independent relaxant responses in young and adult, but not in old, SHR aortas to the levels observed in age-matched WKY, these beneficial effects were more prominent with losartan. Moreover, losartan reduced heart to body weight ratio in all SHR age groups, and selectively in the old WKY group. CONCLUSIONS: Blockade of RAS provides a better protective effect on cardiovascular function compared to sole reduction of blood pressure, and the efficacy of antihypertensive treatment is dictated by age and the hypertensive stage of the animals.     

Pulse pressure, aortic reactivity, and endothelium dysfunction in old hypertensive rats

The reactivity of old hypertensive rat aortas has not been investigated in relation to each phenotype of the blood pressure curve, mean arterial pressure (MAP), and pulse pressure (PP). Aortic reactivities from 3- to 78-week-old Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were studied with the use of organ chambers and invasive blood pressure, carotid diameter, and histomorphometry. MAP and PP were elevated in SHR, but at 78 weeks, a selective increase of PP without further MAP increase was observed for the same carotid diameter as WKY. Aortic relaxation in response to carbamylcholine decreased similarly with age in both strains. With (+) or without (-) endothelium (E), maximal developed tension (MDT) under KCl increased linearly with age in SHR, proportionally to wall thickness and MAP increase. Under norepinephrine (NE), MDT of E(-) aortas from SHR and controls increased with age and reached plateaus at 12 weeks, whereas MDT of E(+) aortas from SHR increased linearly with age. Because the NE-induced MDT was higher for E(-) than E(+), the difference estimated endothelial function. This difference reached plateaus from 12 to 78 weeks in WKY but was abolished beyond 12 weeks in SHR, a finding also observed under NO-synthase inhibition. In old hypertensive rats, (1) increased KCl reactivity is endothelium independent but influenced by the MAP-dependent aortic hypertrophy with resulting increased vascular smooth muscle reactivity, whereas (2) increased NE reactivity is endothelium dependent in association with increased PP, altered endothelial function, and extracellular matrix, with resulting enhanced intrinsic arterial stiffness.     

Antihypertensive and vasodilator actions of antioxidants in spontaneously hypertensive rats

This study was designed to determine whether the antioxidants ascorbic acid, aminotriazole, and glutathione acutely reduce blood pressure (BP) by endothelium-independent or -dependent vasorelaxation in spontaneously hypertensive rats. Blood pressure of male Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) was measured before and 4 h after administration of antioxidants. Thoracic aortic rings with and without endothelium were suspended in organ chambers for isometric tension recordings. Each of the antioxidants, administered in vivo, significantly decreased blood pressure in SHR but had no significant effect on BP in WKY rats. The endothelium-dependent impaired relaxation of SHR aortic rings to acetylcholine (ACh) was improved by prior in vivo administration of each antioxidant. ACh-induced relaxations of aortic rings from WKY was not affected by prior antioxidant treatment. Addition of each antioxidant directly to the organ chamber containing SHR or WKY aortas produced dose- and endothelium-dependent relaxations. Moreover, antioxidant pretreatment of SHR aortic rings significantly potentiated ACh-induced relaxations in these aortas, suggesting that this effect was endothelium dependent. Relaxations induced by the antioxidants alone or by ACh in the presence of antioxidants were inhibited by addition of either xanthine plus xanthine oxidase or nitro-l-arginine. These findings suggest that either excess production of oxidants or a deficiency of antioxidant systems may contribute to the high blood pressure and the endothelium-dependent impairment of vascular relaxation in SHR.     

Intraventricular septal hypertrophy in type 1 diabetic patients with microalbuminuria or early proteinuria

To investigate whether the slightly increased blood pressure that occurs in early diabetic renal disease is associated with hypertensive left ventricular hypertrophy, M-mode echocardiograms were recorded in 11 non-diabetic control subjects and four groups of Type 1 diabetic patients. These were 15 patients without microvascular complications, 10 with microalbuminuria, 12 with early persistent proteinuria, and 8 with established renal impairment. Mean blood pressure was 133/80 mmHg (uncomplicated patients), 143/85 mmHg (microalbuminuria), 147/92 mmHg (early proteinuria) and 158/85 mmHg (renal impairment). Mean intraventricular septal width in the uncomplicated diabetic patients was 9.8 (SE 1.2) mm which did not differ from non-diabetic control subjects. Mean septal width was significantly greater in the other groups (microalbuminuria, 12.7 (1.1) mm, p less than 0.02; proteinuria, 12.0 (0.7) mm, p less than 0.05; renal impairment, 15.5 (1.8) mm, p less than 0.001). Left ventricular mass increased progressively between groups and was significantly increased in those with renal impairment (140 (21) vs 103 (5) g m-2 in uncomplicated patients, p less than 0.05). Septal width in the diabetic population not receiving antihypertensives (n = 37) was significantly correlated with systolic blood pressure (r = 0.45, p less than 0.005) which was the only variable independently related to septal width and ventricular mass. It appears that the slight increase in blood pressure that occurs in microalbuminuria and early proteinuria is frequently associated with hypertensive left ventricular hypertrophy.     

Contractile Responses of Aortae from WKY and SHR to Vasoconstrictors

Aortae taken from spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats aged 4, 8 and 16 weeks were prepared as rings and used to measure the effects of five vasoconstrictors. The endothelium was removed in order to measure selectively the contractile responses induced by potassium chloride (KCl), phenylephrine (PHE), angiotensin‐II (Ang II), endothelin‐1 (ET‐1) and human urotensin‐II (U‐II). These responses were assumed to derive from the activation of specific receptors (namely α₁, AT₁, ET_A and UT‐II) or from depolarization of the smooth muscle fibers by KCl. Specific antagonists prazosin, losartan, BQ‐123 and [Orn⁸]‐UII were used at various concentrations for a pharmacological characterization of these latter receptor systems. The primary purpose of the study was to explore mechanisms or factors that may intervene in the development and maintenance of high blood pressure in SHR. Results indicate that isolated aortae of SHR and WKY contain contractile sites (receptors) whose pharmacological profiles (pEC₅₀ for agonists, pA₂ for antagonists) are very similar to those of other biological systems and should be considered as typical for the α₁, AT₁, ET_A and UT‐II receptor types. Aortae taken from SHR 4 (non hypertensive), 8 and 16 weeks old (hypertensive) responded to the vasoconstrictors with reduced maximal contractions compared to those of age‐matched WKY. These unexpected reduced responses of aortae, observed with the five vasoconstrictors, may be attributed to a non specific lesions. Maximal contraction of aortae from SHR increased from 4 to 16 weeks for KCl, PHE and U‐II, decreased for Ang II, and remained stable for ET‐1. There was also an age‐dependent increase of maximal contraction induced by U‐II in WKY. It is suggested that aortae from SHR undergo early remodelling that leads to reduced contractility in vitro and possibly to vessel rigidity in vivo. The factors involved in this process appear to be of genetic origin since they are present before hypertension: they may contribute to modify aortic compliance and perhaps vascular resistance in hypertensive animals and thus being the cause and not the consequence of high blood pressure.     

Effect of Red Blood Cells and Hemoglobin on Spontaneously Hypertensive and Normotensive Rat Aortas

Experiments were designed to compare the contractile effect of red blood cells (RBC) on aortic rings with and without endothelium from normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Red blood cells of 4 week old WKY and SHR rats induced a negligible increase in tension of aortic rings, either with or without endothelium, being slightly more effective in SHR rats. However, red blood cells of 16 week old rats increased tension of WKY and SHR aortic rings, with endothelium at this age being more pronounced then red blood cells in 4 week old animals. The contractions induced by WKY and SHR red blood cells both in WKY and SHR aortic rings without endothelium at this age are significantly greater compared to the effect on aortic rings with endothelium. Red blood cell ghosts of rats of both strains increased the tension of the rings without endothelium of SHR aorta to near 50% of those induced by red blood cells, whereas they were ineffective in aortic rings without endothelium of WKY rats. Oxyhemoglobin increased the tension of 16 week SHR aortic rings both with and without endothelium, whereas the effect on the rings of WKY rats was negligible. This increase in tension was inhibited by BM 13505, nordihydroguaiaretic acid, and indomethacin in SHR rings both with and without endothelium, demonstrating an eicosanoid involvement in oxyhemoglobin-induced contractions. Hemoglobin or its metabolites may be involved in development or in maintenance of spontaneous hypertensin.     

Low-intensity voluntary running lowers blood pressure with simultaneous improvement in endothelium-dependent vasodilatation and insulin sensitivity in aged spontaneously hypertensive rats.

Our objective is to examine the effects of voluntary running at different intensity levels on blood pressure, endothelium-dependent vessel dysfunction and insulin resistance in aged spontaneously hypertensive rats (SHR) with severe hypertension. Ten-month-old male and female SHR with severe hypertension were assigned to voluntary running at either low intensity (30% of maximal aerobic velocity) or moderate intensity (60% of maximal aerobic velocity) on a motor-driven treadmill for 6 weeks, 20 min per day and 7 days per week. Age-matched Wistar-Kyoto rats and SHR were kept under sedentary conditions as controls. Blood pressure and heart rate were measured by the tail-cuff method. At the end of the exercise training, blood samples were collected for glucose, insulin and lipids assay, and aortae were isolated to examine their function in vitro. Low-intensity but not moderate-intensity running significantly lowered blood pressure in both male and female SHR (p<0.01). There was significant impairment in acetylcholine-induced vasorelaxation in SHR (p<0.01), which was improved by low-intensity training (p<0.05). Nitric oxide synthase blockade abrogated the improvement in endothelium-dependent relaxation. Hypertensive rats had elevated blood glucose and insulin levels with lowered insulin sensitivity that was ameliorated by low-intensity running. A significant increase in blood high-density lipoprotein (HDL)-cholesterol and a significant decrease in triglycerides were found in exercised SHR. In conclusion, low-intensity voluntary exercise lowers hypertension in aged SHR with severe hypertension. Exercise-induced simultaneous improvement in endothelium-dependent vessel relaxation and insulin sensitivity may act concomitantly in attenuating cardiovascular risk factors in aged hypertensive rats with significantly high blood pressure.     

氯沙坦对伴有微量蛋白尿的老年高血压患者的影响

目的　观察氯沙坦对伴有微量蛋白尿（ ＭＣＡ） 的老年高血压患者改善肾损害的作用。　方法　采用连续样本,自身前后及分组对照方法,对３２ 例高血压伴ＭＣＡ 者（ＥＨ 组） ,男２４ 例,女８ 例,平均年龄（７１－６ ±６－８）岁,观察在治疗前和每天服用氯沙坦５０ ｍ ｇ １２ 周后的血压、血尿素氮（ＢＵＮ） 、血肌酐（Ｃｒ） 、２４ｈ 内生肌酐清除率（Ｃｃｒ） 、尿白蛋白／ 肌酐（Ａｌｂ／Ｃｒ） 的变化,ＥＨ 组治疗前在ＢＵＮ、Ｃｒ 、Ｃｃｒ 方面与１２ 例非高血压老人作对照（ 对照组） 。　结果　治疗前ＥＨ 组的Ｃｃｒ 水平较对照组明显降低（ Ｐ＜ ０－０５） ,用氯沙坦治疗后,除血压有明显下降外,尿Ａｌｂ／Ｃｒ 亦显著性降低（ Ｐ＜ ０－０１） ,Ｃｃｒ 明显升高（ Ｐ＜ ０－０５） 。　结论　氯沙坦对老年高血压患者不仅有良好的降压效果,同时可降低尿白蛋白的排泄,改善肾功能