卡托普利对自发性高血压大鼠血压和心肌血管组织肾素血管…

本工作观察了卡托普利对自发性高血压大鼠（ＳＨＲ）血压及心肌，主动脉组织肾素血管紧张素系统（ＲＡＳ）的影响，实验结果表明，ＳＨＲ心肌，主动脉组织血管紧张素Ⅱ含量（ＡＴＩＩ）和血管紧张素换酶（ＡＣＥ）活性显著高于正常血压大鼠（ＷＫＹ）。卡托普列能显著抑制ＳＨＲ心肌，主动脉组织ＡＣＥ活性；降低ＡＴＩＩ含量，并使血压明显降低。提示，血管紧张素转换酶抑制剂（ＡＣＥＩ）对心血管局部组织ＲＡＳ的抑制作用在其降压     

泻肺利水方对自发性高血压大鼠血压的影响

目的通过对服用泻肺利水方的自发性高血压大鼠进行血压监测,以明确该治法及方药的降压疗效。方法选取自发性高血压大鼠50只,应用随机数字表法分为模型组、卡托普利组、中药低剂量组、中药中剂量组、中药高剂量组,每组10只;另取WKY大鼠10只作为正常组。采用全自动大小鼠无创血压测量系统,测量各组灌胃第1天给药前及给药后2、4、6、8h大鼠血压;连续灌胃4周,分别测量1、2、3、4周灌胃后尾动脉压,并进行比较。结果与模型组比较,中药低剂量组给药后2、4h血压明显降低,卡托普利组、中药高剂量组、中药中剂量组给药后2、4、6h血压明显降低,差异有统计学意义(P0.05,P0.01)。中药中剂量组、卡托普利组给药后1、2、3、4周血压明显低于模型组[(207.5±7.5)mmHg、(204.3±8.3)mmHg vs(217.1±11.7)mmHg,(198.1±6.6)mmHg、(195.2±6.3)mmHg vs(215.9±10.8)mmHg,(187.9±5.7)mmHg、(186.0±5.3)mmHg vs(216.8±11.3)mmHg,(177.7±5.3)mmHg、(177.4±5.1)mmHg vs(215.7±13.0)mmHg,1mmHg=0.133kPa,P0.05,P0.01]。中药高剂量组、中药低剂量组给药后2、3、4周血压明显低于模型组(P0.01)。结论泻肺利水方能够有效降低自发性高血压大鼠动脉血压,起效迅速、降压平稳、疗效持久稳定。     

卡托普利对老年高血压患者血尿酸的影响

目的探讨卡托普利对老年高血压患者血尿酸的影响。方法观察55例老年高血压患者服药前后血尿酸、尿素氮(BUN)、肌酐(Cr)、血钾(K     

卡托普利对自发性高血压大鼠心肌纤维化的影响

通过测定自发性高血压大鼠(SHR)左、右心室胶原含量和浓度,观察了高血压情况下心肌间质的改变及卡托普利对其的影响。结果表明,14周龄SHR在血压升高,左室肥厚(LVH)同时,胶原含量亦增加;12周后,治疗组SHR血压显著降低,LVH消退。并且,左、右室胶原浓度分别较未治疗组下降26％及13％,接近正常对照组水平。提示伴随心肌重量增加,SIIR心肌间质亦有胶原纤维异常堆积;卡托普利具有抗纤维化作用,可能通过抑制肾素—血管紧张素—醛固酮系统而实现。     

依那普利与卡托普利对原发性高血压降压疗效的动态血压观察

对50例轻、中度高血压（EH）患者用依那普利（5mg，4／d）和卡托普利（2.5mg，2／d）口服做单盲平等两组对照研究。治疗4周结果两组总有效率相似（分别60.6％，65.2％，P＞0.05），无论SBP和DBP均值的下降均明显（P＜0.05～0.001）。但对每组各抽5例的24h动态血压监测治疗前后比较，依那普利组24h血压控制均较满意，而卡托普利组白天血压控制满意，但夜晚又翌晨血压与治疗前接近（P＜0.05）。如昼夜血压均高者，选用依那普利等长效制剂为佳，如夜间血压正常者，可用卡托普利治疗，唯晨剂应在睡醒后即服为宜。     

早期卡托普利治疗对自发性高血压大鼠阻力血管内皮细胞的影响

用Ｆｏｌｋｏｗ后肢灌流模型来研究阻力血管内皮功能的变化，探讨ＥＤＲＦ／ＮＯ是否参与转换酶抑制剂卡托普利早期治疗ＳＨＲ大鼠防止其高血压的发展。     

太极拳运动对老年高血压的调节作用

目前,国内外均选择一些适合老年人的运动方式来实现高血压的日常防治,国外多倾向于选择游泳、慢跑、步行、骑自行车等运动项目,我国则倾向于选择以太极拳为代表的传统的体育健身方式.太极拳讲究松静自然、形神兼备、圆柔连贯、陶冶情操、修身养性,是一种深得老年人青睐的传统拳种.本文拟探究太极拳运动对老年人高血压的作用,以获得防治高血压的有效方式和手段.     

一氧化氮对老年单纯收缩期高血压大动脉僵硬度及血压的调节作用

老年单纯收缩期高血压大动脉僵硬度增加,一氧化氮参与大动脉僵硬度调节,外源性一氧化氮供体硝酸酯类药物可选择性地降低收缩压,减小脉压。硝酸酯类药物联合传统降压药有助于老年单纯收缩期高血压患者血压控制。     

高血压患者高胰岛素血症与血压的关系及卡托普利对其的影响

对36例原发性高血压患者(EH)、28例正常人分别测定了空腹血糖(BG)、血浆胰岛素(IS)及胰岛素敏感指数(BG/IS)。结果发现EH组血浆IS较正常对照组显著增高(P<0.001);BG/IS显著降低(P<0.001);空腹BG两组间无显著差异;且EH组平均动脉压与血浆IS水平呈显著正相关(r=0.637,P<0.01);与BG/IS呈显著负相关(r=-0.512,P<0.05)。EH组单纯接受卡托普利治疗4周后,血浆IS较治疗前显著降低(P<0.01);BG/IS较治疗前则显著升高(P<0.01)。结果提示:胰岛素抵抗(IR)及高IS血症是致血压升高的重要病生理因素;卡托普利可以改善EH患者的IR及高IS血症。     

槲皮素对野百合碱诱导的大鼠肺动脉高压的影响

目的:观察槲皮素对野百合碱(MCT)诱导的肺动脉高压大鼠的治疗效果。方法:30只成年雄性SD大鼠随机分成3组:MCT诱导的肺动脉高压组(MCT组)、治疗组和对照组。MCT组和治疗组一次性皮下注射MCT 50mg/kg,饲养21d;对照组一次性皮下注射等量0.9%氯化钠溶液,饲养21d。造模后治疗组以槲皮素100mg.kg-1.d-1灌胃20d;MCT组和对照组以0.9%氯化钠溶液2ml/d灌胃20d。20d后,测定3组大鼠平均肺动脉压(mPAP),计算右心室肥大指数(RVHI);光镜下观察大鼠肺组织形态学的改变及肺血管增殖细胞核抗原(PCNA)增殖度的变化,并计算肺中、小动脉管壁厚度占血管外径的百分比(WT%)和肺动脉管壁面积/管总面积的百分比(WA%)。结果:MCT组的mPAP、RVHI、肺中、小动脉WT%、WA%及PCNA增殖度均显著高于对照组及治疗组。结论:槲皮素可降低MCT所致的大鼠肺血管PCNA表达,抑制MCT诱导的肺部炎症、肺血管重建和肺动脉高压形成,对MCT所致的大鼠肺动脉高压具有治疗作用。     

Therapeutic potentials of propolis and pollen on biochemical changes in reproductive function of L-NAME induced hypertensive male rats

Background: Hypertension is described as increased blood pressure based on changed hemodynamics and associated with an increased oxidative damage to reproductive function. This work is to determine therapeutic and protective effects of apitherapy products (propolis and pollen) on reproductive functions of L-NAME-induced hypertensive male rats.

Methods: Experimental animals were indiscriminately separated into four groups of seven rats in each group: (I) Control, (II) L-NAME, (III) L-NAME+ propolis and (IV) L-NAME+ pollen. At the end of the experimental applications, the rats were decapitated by anesthesia and biochemical analyzes were performed on the removed testicular tissues.

Results: The levels of TOS, NF-κB and MDA in the L-NAME group compared to control have increased (p < 0.05). The levels of these parameters in L-NAME+ propolis and L-NAME+ pollen groups compared to the L-NAME group have decreased (p < 0.05). TAS levels, PON1 and CAT activities were significantly decreased in testis tissue samples in the L-NAME-induced group (p < 0.05). However, these parameters were significantly lower in the L-NAME plus propolis and pollen groups (p < 0.05) compared with rats administered L-NAME alone (p < 0.05). NO level significantly reduced (p < 0.05) in L-NAME group compared with control group. There was no statistically significant changes in the NO level of the L-NAME+ propolis group compared with the L-NAME-treated group (p > 0.05).

Conclusion: It has been determined that ethanolic extracts of propolis and pollen, which are natural bee products in the regulation of rising blood pressure. Propolis or pollen is thought to help regulate reproductive function by inhibiting the functioning of inflammatory pathways leading to hypertension.     

Blood pressure variability in established L-NAME hypertension in rats

METHODS: Blood pressure variability was evaluated in conscious Wistar control rats and rats with established L-NAME hypertension (20 mg/kg per 24 h, 4 weeks). RESULTS: Final systolic arterial pressure was 185+/-5 and 132+/-4 mm Hg in the Nomega-nitro-L-arginine methyl ester (L-NAME)-treated and control rats, respectively. The standard deviation of systolic arterial pressure in the L-NAME group was 70% greater than in the control rats, indicating a significant increase in the overall variability. Arterial pressure in the L-NAME rats exhibited aperiodical, abrupt rises and falls and data was grossly non-stationary. Blood pressure variability was therefore evaluated using Poincaré plot analysis. The variance of the difference (delta) between two successive values of systolic arterial pressure, determined for time intervals of 0.2 to 5 s (0.2 s increment), was always significantly higher in the L-NAME group compared with untreated animals. The variance of delta systolic arterial pressure increased with the time interval and plateaued for time intervals of 2.4 and 1.4 s in hypertensive and normotensive rats, respectively. These differences vanished when the sudden events oberved in L-NAME rats were omitted in the construction of Poincaré plots. Acute administration of prazosin (1 mg/kg), but not losartan (10 mg/kg) markedly reduced the variance of delta systolic arterial pressure in hypertensive rats. CONCLUSIONS: Nitric oxide participates in the control of arterial pressure variability. The sympathetic nervous system seems to be a major determinant of the increased short-term variability of arterial pressure in this model.     

Left ventricular failure induced by long-term hypertension in rats

To determine whether the duration of hypertension is an essential component in the evolution of myocardial dysfunction, renal artery constriction was performed in male Fischer 344 rats at 4 months of age, and in vivo global cardiac performance of sham-operated and experimental animals was evaluated 8 months later. Systemic arterial blood pressure increased to 173 +/- 5 mm Hg 2 weeks after the arteries were clipped and remained elevated for the following 5 months. Blood pressure decreased over the remaining 3 months to a value not significantly different from control rats that were killed, 132 +/- 4 mm Hg. After 8 months of renovascular hypertension, we observed that the elevated level of systolic arterial pressure was accompanied by a distinct absence of left ventricular hypertrophy when measured at the ventricular weight level. Moreover, left ventricular end-diastolic pressure increased in hypertensive animals from 6.0 to 24.0 mm Hg while peak left ventricular pressure was identical to controls. In addition, peak +dP/dt and -dP/dt were depressed in hypertensive animals. Although stroke volume was unaltered, cardiac output in renal artery clipped animals was depressed by 34% while total peripheral resistance was elevated by 50%. Ventricular chamber remodeling in the hearts of hypertensive animals was evidenced as a 19% increase in the transverse and a 16% increase in the longitudinal axes of the left ventricle with a 27% diminution of wall thickness. Myocardial damage, in the form of myocyte loss and replacement fibrosis, increased in the hearts of hypertensive animals resulting in a ninefold augmentation in the volume fraction of collagen within the ventricular wall. These alterations in the architectural properties of chamber geometry coupled with the abnormalities in contractile performance resulted in a severe reduction in ejection fraction from 82% to 47% and a marked elevation in transmural diastolic and systolic stress in hypertensive animals. The gradient in stress across the ventricular wall, from epicardium to endocardium, revealed a direct correlation with the regional distribution of myocardial damage. In conclusion, the loading state of the myocardium, tissue injury, and myocardial fibrosis all appear to be critical determinants in the genesis of left ventricular failure in long-term pressure overload.     

老年人睡眠呼吸暂停致高血压的研究进展

阻塞性睡眠呼吸暂停低通气综合征（obstructive sleep apnea hypopnea syndrome，OSAHS）致高血压（hypertension）是临床常见病，对老年人的健康危害很大。流行病学调查、动物实验及临床研究均证明，OSAHS与高血压关系密切。OSAHS是高血压的一个独立危险因素，     

蜂胶黄酮对D-半乳糖致老年痴呆小鼠抗氧化能力的影响

目的 探讨蜂胶黄酮(EEP)对D-半乳糖致老年性痴呆(AD) 小鼠脑指数、脑组织单胺氧化酶B(MAO-B)、超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)的影响.方法 60只健康昆明小鼠随机分成6组,分别为正常组、模型组、阳性对照组及高中低3个剂量蜂胶黄酮治疗组.正常组常规喂养,其余组皮下注射D-半乳糖100 mg·kg-1·d-1,共7 w,阳性对照组造模同时灌胃50 mg·kg-1·d-1茴拉西坦胶囊;治疗组3个剂量(300、150、75 mg·kg-1·d-1)每天灌胃蜂胶黄酮;模型组灌胃等体积的生理盐水.第50天处死小鼠取脑,测其脑指数及脑组织MAO-B,SOD,GSH-Px含量的变化.结果 实验组的脑指数显著高于模型组(P<0.05),SOD,GSH-Px活性显著高于模型组(P<0.01),MAO-B含量显著低于模型组(P<0.01),与正常对照组比较,各指标相近.结论 蜂胶黄酮能提高脑指数,增强抗氧化能力,抑制MAO-B活性,从而保护脑细胞,抵抗痴呆.     

Enhanced expression of Gi proteins in non-hypertrophic hearts from rats with hypertension-induced by L-NAME treatment

OBJECTIVE: The objective of the present studies is to investigate if the enhanced expression of Gs alpha protein and their mRNA observed in various models of hypertensive rats is due to the expressed hypertrophy or hypertension. METHODS: Hypertension, in Sprague-Dawley rats was induced by the oral administration of the arginine analog N(omega)-nitro-L-arginine methyl ester (L-NAME) in their drinking tap water for a period of 4 weeks. The control rats were given plain tap water only. The levels of inhibitory guanine nucleotide regulatory proteins (Gi alpha-2, Gi alpha-3), stimulatory guanine nucleotide proteins (Gs alpha) and G beta proteins were determined by immunoblotting, whereas the levels of Gi alpha-2, Gi alpha-3, Gs alpha and adenylyl cyclase type V enzyme mRNA were determined by Northern-blotting techniques. Adenylyl cyclase activity was determined by measuring [32P]cAMP formation from [alpha32P]ATP. RESULTS: The systolic blood pressure was enhanced in L-NAME-treated rats compared to control rats (190 +/- 9.2 mmHg versus 121 +/- 6.3 mmHg); however, heart-to-body-weight ratio was not different in two groups. The levels of Gi alpha-2 and Gi alpha-3 proteins and their mRNA were significantly augmented in hearts from L-NAME-treated rats, however, the levels of Gs alpha and G beta were unaltered. In addition, the effect of low concentrations of GTPgammaS on forskolin (FSK)-stimulated adenylyl cyclase activity (receptor-independent functions of Gi alpha) was significantly enhanced in L-NAME-treated rats. However, the inhibitions of adenylyl cyclase exerted by oxotremorine, C-ANP(4-23) and angiotensin II (AII) (receptor-dependent function of Gi alpha) were completely attenuated in L-NAME-treated rats. On the other hand, cholera toxin stimulated GTP or GTPgammaS-sensitive adenylyl cyclase activity (Gs alpha function) to similar extent in control and L-NAME-treated rats, suggesting that Gs alpha functions were not altered by L-NAME treatment. However, the stimulatory effects of isoproterenol, glucagon, NaF on adenylyl cyclase were diminished in L-NAME-treated rats. In addition, FSK-stimulated enzyme activity was also diminished in L-NAME-treated rats without any changes in the mRNA levels of type V enzyme. CONCLUSIONS: These results suggest that L-NAME hypertensive rats that do not express cardiac hypertrophy exhibit enhanced expression of Gi alpha protein and associated adenylyl cyclase activity.     

Aldehyde induced hypertension in rats: prevention by N-acetyl cysteine

Methylglyoxal, a highly reactive endogenous aldehyde is formed in the tissue of humans and animals as an intermediate of glucose and fructose metabolism. N-acetyl cysteine (NAC), an analogue of the dietary amino acid cysteine, binds aldehydes thus preventing their damaging effect on physiological proteins. We measured systolic blood pressure (SBP), platelet [Ca2+]i, circulating nitric oxide levels, tissue aldehyde conjugates and renal vascular changes in chronic methyglyoxal treated Wistar-Kyoto (WKY) rats and examined the effect of NAC in the diet on these parameters. Animals, age seven weeks, were divided into three groups of six animals each and were treated as follows: WKY-control (chow diet and normal drinking water); WKY-methylglyoxal (chow diet and methyglyoxal in drinking water); WKY-methyglyoxal + NAC (1.5% NAC in diet and methylglyoxal in drinking water) for the next 18 weeks. Methylgyoxal in drinking water was given at a concentration of 0.2% during weeks 0-5; 0.4%, weeks 6-10; and 0.8%, weeks 11-18. After 18 weeks systolic blood pressure, platelet [Ca2+]i and kidney aldehyde conjugates were significantly higher and serum nitric oxide levels lower in methylglyoxal treated rats. Methylglyoxal treated rats also showed smooth muscle cell hyperplasia in the small artery and arterioles of the kidney. N-acetyl cysteine, an aldehyde binding thiol compound, prevented these changes.     

Effects of omapatrilat on blood pressure and renal injury in L-NAME and L-NAME plus DOCA-treated rats

BACKGROUND: This study investigates the effects of chronic administration of omapatrilat (OMA) on blood pressure (BP), renal injury, and other variables in N(omega)-nitro-L-arginine methyl ester (L-NAME) hypertension and in the low-renin model produced by the simultaneous administration of L-NAME and deoxycorticosterone acetate (DOCA). METHODS: The control, DOCA, L-NAME, L-NAME + DOCA, L-NAME + OMA, and L-NAME + DOCA + OMA groups were used. Tail systolic BP was measured twice a week. After 4 weeks of treatment, mean arterial pressure (MAP), and metabolic, morphologic, and renal variables were measured. RESULTS: The final values of MAP were 109 +/- 5.1 mm Hg for the control group, 113 +/- 3.0 mm Hg for DOCA, 175 +/- 3.7 mm Hg for L-NAME, 193 +/- 3.8 mm Hg for L-NAME + DOCA, 117 +/- 3.9 mm Hg for L-NAME + OMA, and 158 +/- 3.0 mm Hg for L-NAME + DOCA + OMA. The rats treated with L-NAME showed mild and scarce renal lesions, which were prevented by OMA treatment and the L-NAME + DOCA group showed proteinuria and hyaline arteriopathy, which were markedly attenuated in the L-NAME + DOCA + OMA group. Plasma urea and creatinine were significantly increased in the L-NAME + DOCA group, whereas these variables were not significantly greater in the L-NAME + DOCA + OMA group versus controls. The L-NAME + DOCA group showed relative renal and cardiac hypertrophy that was not observed in the L-NAME + DOCA + OMA group. CONCLUSIONS: The simultaneous blockade of neutral endopeptidase (NEP) and angiotensin converting enzyme (ACE) completely prevents L-NAME hypertension. Our results also show that OMA attenuates the increased BP and the renal injury in L-NAME hypertensive rats treated with DOCA. Assuming that this is a low-renin model of hypertension, the protective effect of OMA may be due to an increase in vasodilator peptides produced by both ACE and NEP inhibition.