哇巴因抗体对肾血管性高血压大鼠的降压作用

目的：探讨哇巴因抗体的降压作用及内源性哇巴因与高血压发病的关系。方法：给”一肾一夹（１Ｋ１Ｃ）“”两肾一夹＋盐（２Ｋ１Ｃ－ｓａｌｔ）”肾血性高血压大鼠随机静注哇巴因抗体、硝普钠、正常兔免疫球蛋白（ＩｇＧ）及生理盐水,颈动脉插管观察注射生３小时内大鼠血压的动态变化。结果：哇巴因抗体对“一肾一夹”、“两肾一夹＋盐”型高血压大鼠具有明显的降压作用,而对“两肾一夹”高血压鼠降压作用不明显。正常免免疫球蛋白     

哇巴因的升压作用及哇巴因抗体对高血压大鼠血压的影响

目的 :探讨内源性哇巴因在高血压发病中的作用。　　方法 :分别给予正常 SD大鼠每天腹腔注射外源性哇巴因 (2 5μg/kg,哇巴因组 )及等量生理盐水 (对照组 ) ,观察用药10周血压的动态变化 ;“一肾一夹”高血压大鼠分别给予舌下静脉注射哇巴因抗体 (哇巴因抗体组 )、生理盐水 (生理盐水组 )及正常兔免疫球蛋白 G(正常兔 Ig G组 ) ,颈动脉插管监测血压 ,观察用药后 3小时内血压的动态改变。　　结果 :与对照组比较哇巴因组大鼠注射哇巴因后 3周血压即开始升高 [12 0 .5± 15 .4mm Hg比 10 9.4± 11.8mm Hg(1mm Hg=0 .133 k Pa) ,P<0 .0 5 ],第 10周时血压明显高于对照组 (143.6± 17.3 mm Hg比 12 1.3± 15 .3 mm Hg,P<0 .0 1) ;哇巴因抗体对“一肾一夹”高血压大鼠具有明显的降压作用 ,而正常兔 Ig G组与生理盐水组比较降压作用不明显。　　结论 :体内哇巴因含量升高可能是高血压发病因素之一 ,在血压升高中发挥着较为重要的作用。     

双肾双夹大鼠肾血管性高血压模型的制作

目的:探讨用自制铝夹狭窄双肾动脉(2K2C)复制大鼠肾血管性高血压模型的方法。方法:选用SD大鼠64只,随机分为假手术(sham)4周(4w)组和8周(8w)组及手术(2K2C)4w组和8w组。用无创动物血压测试仪测量各组大鼠尾动脉血压值。术后4w或8w时处死动物,称左心室重(LVW)和体重(BW),计算左室重量指数(LVW/BW)。结果:2K2C术后2w血压即明显升高,显著高于sham组(P<0.01),术后4w血压继续上升,血压值稳定在(157.63±14.13)mmHg,术后8w血压值高达(177.98±18.03)mmHg。sham组手术前后血压值无明显变化。2K2C-4w组和2K2C-8w组LVW、LVW/BW较同时间sham组显著增加(P<0.01)。结论:采用自制铝夹能成功复制肾血管性高血压,血压升高显著且稳定,成功率高,重复性好,方法简便易行。     

易卒中型肾血管性高血压大鼠的心脏损害

通过观察易卒中型肾血管性高血压大鼠心脏的病理形态．发现所有高血压大鼠均有不同程度的左心室肥厚和心肌内小冠状动脉病变，但大冠状动脉无粥样硬化，在此基础上自发性心肌梗塞率为41．8％。表明心室肥厚和心肌内小冠状动脉病变在高血压所致的心肌缺血性损害中起重要作用。     

心钠素对肾血管性高血压的临床作用

肾血管性高血压有复杂的病理生理特点,适于全面评价心钠素的生理、药理作用。给7例患者静脉滴注心钠素0.025μg·kg~(-1)/min×60min,引起肾素—血管紧张素—醛固酮系统及交感神经系统的抑制,血浆加压素浓度的降低,产生了利尿、利钠效应并伴有红细胞压积和肌酐清除率的增加,血压轻度平续的下降。一些因素参与了肾血管性高血压的形成和维持。本研究提示,心钠素对这些因素均有一定作用     

17β-雌二醇对肾血管性高血压大鼠心肌肥厚的影响

临床和动物实验证实 ,雌激素替代治疗具有心脏保护作用[1 ] 。我们采用两肾一夹 +双侧去卵巢的绝经动物模型 ,来观察雌激素对肾动脉狭窄所致的高血压大鼠心脏保护作用 ,并探讨其可能的机制。1　材料与方法将体重 15 0～ 2 0 0g的 8～ 10周龄清洁级雌性Wistar大鼠5 0只 ,随机分为两组 ,1组 4 4只 ,给予左侧肾动脉钳夹术 ;另1组 6只 ,给予相应假手术对照 ,即对照组。 4周后 ,将血压持续超过 15 0mmHg(1mmHg =0 .133kPa)而且精神状态较好的大鼠随机分为两组 ,1组给予去卵巢术 ,另 1组给予相应假手术 ,即假去势组。将去卵巢的大鼠随机分为两组…     

双肾双夹易卒中型肾血管性高血压大鼠重要靶器官小窝蛋白的表达

目的 研究在高血压发展过程中重要靶器官组织信号蛋白小窝蛋白（Caveolin-1）的表达。方法 建立双肾双夹易卒中型肾血管性高血压大鼠动物模型，随机分为高血压组和假手术组，用Western blot的方法检测小窝蛋白在心、脑、肾血管中的表达。结果 2周末高血压组血压明显升高，4周末高血压组心脏体重比明显升高，高血压组重要靶器官心、脑、肾、血管中小窝蛋白的表达随高血压的时程发展明显减少。结论 双肾双夹易卒中型肾血管性高血压大鼠重要靶器官组织小窝蛋白表达减少，提示小窝蛋白信号途径可能参与高血压的发生发展，与高血压靶器官的损害有关。     

肾血管性高血压

病史患者男性，35岁，因“发现高血压5年，尿检异常10余天”于2003-03-26入院。     

Apelin在肾血管性高血压大鼠模型中的浓度及意义

目的观察Apelin在肾血管性高血压大鼠模型中的含量以及与血管紧张素Ⅱ(AngⅡ)、一氧化氮(NO)的相关性,探讨Apelin在肾血管性高血压中的作用。方法将20只雄性180～220gWistar大鼠随机分为手术组和假手术组。在术后4周测量平均颈动脉压,确定模型制备成功。ELISA法测定血浆Apelin-12、AngⅡ、NO浓度,分析其相关性;免疫组化法检测心脏Apelin-12蛋白表达。分析手术组与假手术组平均颈动脉压、血浆Apelin-12、AngⅡ、NO浓度变化和心脏组织Apelin-12表达情况。结果平均颈动脉压手术组与假手术组相比显著增高(P<0.01)。血浆中Apelin-12及AngⅡ浓度手术组高于假手术组(P<0.01);血浆中NO浓度手术组低于假手术组(P<0.01)。心脏组织中Apelin-12蛋白表达手术组高于假手术组。手术组血浆中Apelin-12浓度与AngⅡ浓度呈正相关(r=0.877,P<0.01),与NO浓度呈负相关(r=-0.853,P<0.01)。结论 Apelin-12可能在肾血管性高血压的病理生理发展过程中发挥作用。Apelin-12、AngⅡ、NO共同参与肾血管性高血压的发生发展过程,Apelin-12可能通过AngⅡ、NO发挥作用。     

金线莲提取物ARL对肾血管性高血压大鼠血压、血管紧张素Ⅱ、一氧化氮和内皮素的影响

目的观察金线莲提取物ARL对肾血管性高血压大鼠(RHR)血压、血浆血管紧张素Ⅱ(AngⅡ)、内皮素(ET-1)和血清一氧化氮(NO)、一氧化氮合酶(NOS)浓度的影响。方法应用二肾一夹法制作RHR模型。ARL灌胃给药15 d,给药后第5、10、15天以大鼠尾动脉测压法测量清醒 RHR收缩压及心率。给药第15天末处死动物取血,放射免疫法测AngⅡ、ET-1浓度,硝酸还原酶法、生物化学法分别测定血清NO、NOS浓度。结果ARL灌胃给药5 d后,RHR的血压和心率较给药前明显降低。ARL给药15 d后,RHR血清NO、NOS的含量明显增加、血浆ET-1、AngⅡ的含量明显降低。结论ARL对肾血管性高血压大鼠具有良好的降压作用,其降压机制可能与降低ET-1、AngⅡ升高NO的含量有关。     

罗格列酮对自发性高血压大鼠的降压作用

目的 为了初步了解胰岛素增敏剂罗格列酮对自发性高血压大鼠的降压作用和机理，设计了本项实验。方法 自发性高血压大鼠36只，随机分为3组，罗格列酮和硝苯吡啶分别作为观察药和阳性对照药添加到大鼠饮水中，另有一组空白对照。结果 2种药物均呈现显著的降压作用，但血胰岛素水平测量结果没有达到显著的统计学差异。结论 胰岛素增敏剂—罗格列酮可以显著降低自发性高血压大鼠的血压，其机理有待深入探讨。     

罗格列酮对自发性高血压大鼠的降压作用

目的为了初步了解胰岛素增敏剂罗格列酮对自发性高血压大鼠的降压作用和机理,设计了本项实验.方法自发性高血压大鼠36只,随机分为3组,罗格列酮和硝苯吡啶分别作为观察药和阳性对照药添加到大鼠饮水中,另有一组空白对照.结果 2种药物均呈现显著的降压作用,但血胰岛素水平测量结果没有达到显著的统计学差异.结论胰岛素增敏剂-罗格列酮可以显著降低自发性高血压大鼠的血压,其机理有待深入探讨.     

Effects of Chronic Exercise on Blood Pressure in Dahl Salt-Sensitive Rats

We tested the hypothesis that daily exercise would reduce directly measured arterial blood pressure (BP) and sympathetic nervous system support of BP in conscious, unrestrained, female Dahl salt-sensitive rats consuming 4.0% NaCl. Dahl S/Jr inbred rats were assigned to daily exercise (EX) or sedentary (SED) treatment conditions (n = 12/group) at 4 weeks of age. Rats in the EX group were housed in cages with attached running wheels. After 5 weeks of exercise, rats were running 10.3 ± 1.7 km/day. After at least 5 wks of treatment, all rats in both groups were placed on a 4.0% NaCl diet for 2 weeks to produce sodium-induced hypertension. Rats continued to either exercise daily or remain sedentary for an additional 2 weeks while consuming the high sodium diet. Carotid and jugular catheters were then implanted for measurements in conscious, resting, unrestrained rats on two separate days. Daily wheel running exercise for 7 to 9 weeks did not alter BP or HR in Dahl S/Jr rats consuming a 4.0% NaCl diet. However, acute arterial depressor responses to ganglionic blockade were less in EX rats. Furthermore, greater α-adrenergic (phenylephrine-induced) pressor responses were observed in the EX group while under ganglionic blockade. The findings suggest that overall resting sympathetic neural activity or cardiac β-adrenergic responsiveness to sympathetic activity is reduced in this model of hypertension by daily wheel running exercise.     

四逆汤(附子、干姜、甘草)对肾血管性高血压大鼠血压调节作用的实验研究

目的 探讨四逆汤对肾血管性高血压大鼠血压的调节作用和可能的机制.方法 健康雌性Wistar大鼠24只,随机分为正常组、对照组和治疗组,每组8只.根据双肾动脉夹闭法建立肾性高血压动物模型,应用四逆汤(附子、干姜、甘草)灌胃治疗2周,RBF-2型鼠尾动脉血压计测量血压,放射免疫法测定血浆中血管紧张素Ⅱ(Ang Ⅱ)和降钙素基因相关肽(CGRP)的含量,TUNEL法检测肾组织细胞凋亡,免疫组化法测定肾组织中Ang Ⅱ和CGRP的表达.结果 (1)对照组和治疗组大鼠血压较正常组明显升高,四逆汤能明显降低血压[(131.6±14.2 vs 116.2±8.3)mm Hg,P＜0.05].(2)各组动物血浆AngⅡ水平无显著性变化(P＞0.05),治疗组CGRP含量较对照组明显升高[(75.2±12.2 vs 54.8±18.1)pg/mL,P＜0.05].(3)四逆汤治疗明显减少肾小球凋亡阳性细胞数(12.6±3.5 vs 29.4±3.5细胞个数/10个视野, P＜0.05);治疗组明显降低AngⅡ表达水平,显著升高CGRP表达水平(P＜0.05).结论 四逆汤可能通过调节肾血管性高血压大鼠血浆和肾组织中血管活性物质Ang Ⅱ和CGRP的水平,发挥其血压调节和保护高血压靶器官的作用.     

四逆汤(附子、干姜、甘草)对肾血管性高血压大鼠血压调节作用的实验研究

目的探讨四逆汤对肾血管性高血压大鼠血压的调节作用和可能的机制。方法健康雌性Wistar大鼠24只,随机分为正常组、对照组和治疗组,每组8只。根据双肾动脉夹闭法建立肾性高血压动物模型,应用四逆汤(附子、干姜、甘草)灌胃治疗2周,RBF-2型鼠尾动脉血压计测量血压,放射免疫法测定血浆中血管紧张素Ⅱ(AngⅡ)和降钙素基因相关肽(CGRP)的含量,TUNEL法检测肾组织细胞凋亡,免疫组化法测定肾组织中AngⅡ和CGRP的表达。结果(1)对照组和治疗组大鼠血压较正常组明显升高,四逆汤能明显降低血压[(131.6±14.2vs116.2±8.3)mmHg,P<0.05]。(2)各组动物血浆AngⅡ水平无显著性变化(P>0.05),治疗组CGRP含量较对照组明显升高[(75.2±12.2vs54.8±18.1)pg/mL,P<0.05]。(3)四逆汤治疗明显减少肾小球凋亡阳性细胞数(12.6±3.5vs29.4±3.5细胞个数/10个视野,P<0.05);治疗组明显降低AngⅡ表达水平,显著升高CGRP表达水平(P<0.05)。结论四逆汤可能通过调节肾血管性高血压大鼠血浆和肾组织中血管活性物质AngⅡ和CGRP的水平,发挥其血压调节和保护高血压靶器官的作用。     

Apelin Effects on Blood Pressure and RAS in DOCA-Salt-Induced Hypertensive Rats

Apelin, a novel multifunctional peptide implicated in the regulation of the cardiovascular system, including blood pressure and cardiac function control, has been postulated to be involved in the pathophysiology of hypertension and hypertensive heart disease. The aim of this study was to investigate, for the first time, whether the effects of apelin’s chronic application might be involved in deoxycorticosterone acetate-salt-induced hypertensive rats (DOCA-salt rats). In this study, 8–10-week-old male Wistar rats were divided into four groups: control, control + apelin, DOCA-salt rats, DOCA-salt rats + apelin. Deoxycorticosterone Acetate (25 mg/kg of body weight) was injected subcutaneously, twice a week for 4 weeks. These rats received NaCl 1% instead of tap water for drinking during the experimental period. Later, rats were randomly treated with pyroglutamylated apelin-13 (200 μg. kg^?1. day^?1 intraperitonealy) for 17 days. The concentrations of apelin, endothelin-1, angiotensin-converting enzyme, angiotensinogen, and angiotensin II were analyzed in the plasma. The mRNA level of apelin and apelin receptor were determined in the heart and aorta tissue by real-time polymerase chain reaction, respectively. It was found that apelin reduces blood pressure in DOCA-salt rats. Apelin can be used as a therapeutic agent in the treatment of hypertension in the future.     

Effects of Chronic Arachidonate on Blood Pressure of Spontaneously Hypertensive Rats

Three weeks of treatment with arachidonic acid (250 mg/kg/day, s.c.) produced an antihypertensive effect in 16 week-old spontaneously hypertensive rats (SHR) as compared with vehicle treated rats. Indomethacin (4 mg/kg, s.c. B.I.D.), given concurrently with arachidonate, abolished the antihypertensive effect. Plasma catecholamines were not altered by the arachidonate treatment, but blood pressure increments after spinal cord stimulation or after intravenous administration of norepinephrine and angiotensin II in the pithed rat were diminished. Increments in plasma catecholamines in response to spinal cord stimulation were similar in both groups of pithed rats.

These data demonstrate the antihypertensive effect of arachidonic acid in SHR with established hypertension. This beneficial effect seems to be mediated through cyclooxygenase metabolites, and might be related to reduced responsiveness of peripheral blood vessels to pressor stimuli.