缬沙坦的降压和肾脏保护作用研究

目的 观察血管紧张素Ⅱ受体拮抗剂（ARB）缬沙坦对原发性高血压伴早期2型糖尿病肾病患者的降压效果和肾脏保护作用。方法 轻、中度原发性高血压伴早期2型糖尿病肾病患者入选本实验并随机分为缬沙坦组和培他乐克加安体舒通组。于4w末根据血压调整剂量和疗程，6m后对患者进行评价。结果 两组的降压及副作用相似。缬沙坦组和培他乐克加安体舒通组在治疗后24h尿白蛋白排泄率（24hUAER)水平和24hUAER的降低幅度有显著性差异（P＜0.05)。其余指标无显著性差异（P＞0.05)。结论 缬沙坦治疗轻、中度原发性高血压的有效率和培他乐克加安体舒通近似且耐受性好。作为一种强力高选择性的血管紧张素Ⅱ型受体拮抗剂，缬沙坦可以减慢早期2型糖尿病肾病蛋白尿的进展，并具有肾脏保护作用。     

缬沙坦的降压和肾脏保护作用研究

目的 观察血管紧张素Ⅱ受体拮抗剂(ARB)缬沙坦对原发性高血压伴早期2型糖尿病肾病患者的降压效果和肾脏保护作用。方法 轻、中度原发性高血压伴早期2型糖尿病肾病患者入选本实验并随机分为缬沙坦组和培他乐克加安体舒通组。于4w末根据血压调整剂量和疗程,6m后对患者进行评价。结果 两组的降压及副作用相似。缬沙坦组和培他乐克加安体舒通组在治疗后24h尿白蛋白排泄率(24hUAER)水平和24hUAER的降低幅度有显著性差异(P<0.05)。其余指标无显著性差异(P>0.05)。结论 缬沙坦治疗轻、中度原发性高血压的有效率和培他乐克加安体舒通近似且耐受性好。作为一种强力高选择性的血管紧张素Ⅱ型受体拮抗剂,缬沙坦可以减慢早期2型糖尿病肾病蛋白尿的进展,并具有肾脏保护作用。     

缬沙坦对降血压和保护肾脏的作用研究

目的 观察血管紧张素Ⅱ受体拮抗剂(ARB)缬沙坦对原发性高血压伴早期糖尿病肾病患者的降压效果和肾脏保护作用.方法 轻、中度原发性高血压伴早期糖尿病肾病患者100例随机分为缬沙坦组和美托洛尔加氢氯噻嗪组各50例.根据血压调整剂量和疗程,6个月后对两组血压及24h尿白蛋白排泄率进行对比.结果 两组的降压及副作用差异无统计学意义(P0.05).缬沙坦组和美托洛尔加氢氯噻嗪组在治疗后24h尿白蛋白排泄率(24hUAER)水平和24hUAER的降低幅度方面比较差异有统计学意义(均P<0.05),其余指标差异无统计学意义(P0.05).结论 缬沙坦治疗轻、中度原发性高血压的有效率和美托洛尔加氢氯噻嗪近似且耐受性好,可以减慢早期糖尿病肾病的进展而具有肾脏保护作用.     

氯沙坦的降压效应和肾脏保护作用研究

目的观察血管紧张素Ⅱ受体拮抗剂(ATRa)氯沙坦对有早期2型的肾病、糖尿病及原发性高血压的患者产生的降压效果及对肾脏的保护效果。方法选择200例符合要求的患者,分成氯沙坦组和培他乐克加安体舒通组,于5周末根据血压调整剂量和疗程,4个月后对患者进行评价,对试验数据用SPSS18.0进行分析。结果在降压及副作用方面,两组的结果相似;在氯沙坦和培他乐克加安体舒通两组比较中,在治疗24h后的尿白蛋白排泄率(24hUAER)水平和24hUAER的降低幅度两方面比较,差异有统计学意义(P0.05),其余指标比较,差异无统计学意义(P0.05)。结论氯沙坦治疗轻、中度原发性高血压的有效率和培他乐克加安体舒通近似且耐受性好;氯沙坦是血管紧张素Ⅱ受体的拮抗剂,它具有选择性高、专属性强的效果,对早期糖尿病、肾病形成蛋白尿的进度起到减缓作用,同时也有保护肾脏的作用。     

非洛地平与缬沙坦对原发性高血压肾脏保护作用的对比研究

目的探讨非洛地平与缬沙坦对原发性高血压患者肾脏的保护作用。方法将我院2011年2月至2012年3月收治的56例原发性高血压伴蛋白尿患者随机分为A组、B组,每组28例。A组给予非洛地平,B组给予缬沙坦,疗程为3个月,比较两组药物的治疗效果。结果两组患者治疗后血压与治疗前相比,差异均有统计学意义(P<0.01);但治疗后两组血压相比差异无统计学意义(P>0.05);两组患者治疗后24 h蛋白尿与治疗前相比,差异均有统计学意义(P<0.01);但治疗后两组24 h蛋白尿比较差异无统计学意义(P>0.05)。结论非洛地平和缬沙坦均具有显著的降压作用,可保护原发性高血压患者肾脏功能,但非洛地平价格明显低于缬沙坦,有望成为广大基层医院原发性高血压的首选肾脏保护药物。     

缬沙坦和雷米普利对原发高血压患者肾脏保护作用的对比研究

目的研究缬沙坦和雷米普利对原发高血压患者肾脏的保护作用。方法 84例对原发高血压患者随机分为缬沙坦和雷米普利组,治疗时间为10周,观察两组患者治疗前后血压、血尿素氮（BUN）、尿白蛋白及N-乙酰基-葡萄糖苷酶（NAG）的变化。结果治疗后两组患者的血压尿白蛋白和NAG均较前明显下降（P〈0.05）,且两组相比比较无统计学差异（P〈0.05）。结论缬沙坦和雷米普利对原发高血压患者肾脏均明显保护作用。     

缬沙坦和金水宝对糖尿病肾病的保护作用

目的：观察缬沙坦和金水宝胶囊治疗糖尿病肾脏病（DKD）IV期患者的疗效。方法：将入选的36例患者随机分为A、B两组,两组均控制血糖和血压,在此基础治疗上两组均服用缬沙坦,B组加服金水宝胶囊。结果：两组治疗后24h尿蛋白均明显下降（P〈0．05）,且B组更显著（P〈0．05）;A组治疗前后血肌酐（SCr）、尿素氮（BUN）、血胆固醇（TC）、甘油三酯（TG）相比差异无显著性（P〉0．05）,B组治疗后均下降,与治疗前比差异有显著性（P〈0．05）。结论：缬沙坦和金水宝胶囊是治疗DKD的有效药物,金水宝还有降低SCr、BUN、TC、TG的作用,二者联用,可更有效延缓DKD的进展。     

缬沙坦及贝尼地平对原发性高血压伴蛋白尿患者肾脏保护作用的研究

目的探讨缬沙坦与贝尼地平对原发性高血压伴蛋白尿患者的疗效及保护肾脏差别。方法随机选取2009年1月至2011年1月就诊我院的原发性高血压伴蛋白尿患者286例,分为A组(143例)和C组(143例),分别采用缬沙坦与贝尼地平治疗24周,对比两组患者治疗后的高血压总有效率、血清肌酐、肌酐清除率、尿微量蛋白的变化情况。结果经治疗后,两组患者血压控制总有效率相似,肌酐清除率均升高,血清肌酐及尿微量蛋白均降低,两组之间差异无统计学意义,P>0.05。结论缬沙坦及贝尼地平均能通过不同的途径有效地控制血压,保护肾脏,且疗效相当。     

小剂量阿托伐他汀联合缬沙坦对早期糖尿病肾病的肾脏保护作用

目的探讨小剂量阿托伐他汀联合缬沙坦对早期糖尿病肾病的肾脏保护作用。方法选取520例在我院就诊的早期2型糖尿病肾病患者,随机分为观察组(阿托伐他汀+缬沙坦)和对照组(缬沙坦)各260例。对比24 h尿白蛋白排泄率(UAER)、C反应蛋白(CPR)、糖化血红蛋白(HbA_1c)、总胆固醇(TC)、三酰甘油(TG)、尿素氮(BUN)、血肌酐(SCr)及药物不良反应。结果治疗前两组UAER、CPR、HbA_1c、TC、TG、BUN、SCr水平比较,差异无统计学意义(P>0.05)。治疗后观察组UAER、CPR、TC、TG、BUN和SCr水平均显著低于治疗前(P<0.05),而HbA_1c水平和治疗前比较,差异无统计学意义(P>0.05);对照组UAER、CPR、BUN和SCr水平均显著低于治疗前(P<0.05),而HbA_1c、TC和TG水平和治疗前比较,差异无统计学意义(P>0.05)。观察组UAER、CPR、TC和TG水平显著低于对照组(P<0.05),但两组HbA_1c、BUN和SCr水平比较,差异无统计学意义(P>0.05)。观察组不良反应率9.62%与对照组8.85%比较,差异无统计学意义(P>0.05)。结论早期糖尿病肾病应用小剂量阿托伐他汀联合缬沙坦治疗更能有效的减少蛋白尿,对肾脏具有保护作用,且安全性良好。     

缬沙坦的降压作用及对心脏的保护

目的观察缬沙坦对60例高血压患者的降压作用及其对心脏的保护。方法设置治疗组和对照组,治疗组口服缬沙坦治疗,运用24h动态血压监测,并采用心电图、心脏彩超、心脏三位片等观察左心室情况．结果缬沙坦能有效降低昼夜血压,并能逆转心室重构,改善心室的顺应性。结论缬沙坦能有效降压,对心脏有保护作用。     

盐酸埃他卡林选择性降压作用的研究

目的 :在清醒正常血压犬和“两肾一夹”肾性高血压犬 (RHD)上 ,观察不同剂量盐酸埃他卡林(iptakalimhydrochloride,Ipt)的降压作用特征 ;在清醒正常血压的Wistar大鼠和脑卒中易感型自发性高血压大鼠 (stroke pronespontaneouslyhypertensiverat,SHRsp)上 ,采用无创心功能监测方法 ,观察Ipt对心功能和血流动力学的作用特征 ,以判断其降压作用和对心功能及血流动力学的影响是否具有选择性。方法 :给清醒正常血压犬和RHD口服不同剂量的Ipt,用听诊法测量移于皮鞘内的颈总动脉血压 ,用触诊法测量心率 ,同时记录Ⅱ导联心电图。给清醒正常血压大鼠和SHRsp静脉注射相同剂量的Ipt,采用清醒无创心功能血流动力学实验方法 ,观察Ipt对对心功能和血流动力学的影响。结果 :在RHD模型上 ,单次口服Ipt0 .1 2 5、0 .2 5、0 .5、1 .0mg·kg- 1 后 ,产生剂量依赖性的降压作用 ,0 .5h开始起效 ,2～ 3h达效应峰值 ,其最大降低SBP幅度分别为 1 3、2 3、2 5、3 6mmHg,降压作用维持时间分别为 4、6、6、1 2h。在清醒正常血压犬上 ,单次口服Ipt 0 .8,3 .2 ,1 2 .8mg·kg- 1 ,其中剂量为 0 .8和 3 .2mg·kg- 1 时 ,血压和心率均无明显变化 ,剂量增至 1 2 .8mg·kg- 1 时 ,在给药后 5h之内可以显著降低收缩压和舒张压 ,其最大降低SB     

Mechanisms responsible for renoprotective effects of renin-angiotensin inhibitors

In recent years, the focus of interest on the role of the renin-angiotensin system (RAS) in the pathophysiology of hypertension and organ injury has changed to a major emphasis on the role of the local RAS in specific tissues. In the kidney, all of the RAS components are present and intrarenal angiotensin II (Ang II) is formed by independent multiple mechanisms. Ang II is compartmentalized in the renal interstitial fluid and the proximal tubular compartments with much higher concentrations than those existing in the circulation. It has also been revealed that inappropriate activation of the intrarenal RAS is an important contributor to the pathogenesis of chronic kidney disease (CKD). Indeed, most national guideline groups now recommend the use of RAS inhibitors in preference to other antihypertensive agents for hypertensive patients with CKD. In this review, we will briefly summarize our current understanding of independent regulation of the intrarenal RAS. We will also discuss the impact of RAS inhibitors in preventing the progressive increases in the intrarenal RAS during the development of CKD.     

Combination antihypertensive therapy with valsartan and hydrochlorothiazide in Chinese patients with mild-to-moderate hypertension

ABSTRACT

Objectives: To compare the efficacy and safety of valsartan (VAL)/ HCTZ 80/12.5?mg with VAL 80?mg in Chinese patients with mild-to-moderate essential hypertension not adequately controlled with VAL 80?mg alone.

Research design and methods: This was a multicenter, double-blind, double-dummy, randomized, active-controlled, parallel-group trial. Patients (1175) with mild-to-moderate essential hypertension (mean sitting diastolic blood pressure [MSDBP] ≥?95 and <?110?mmHg) from 26 centers in China received VAL 80?mg o.d. for 4?weeks, 864 patients whose MSDBP remained ≥?90 and <?110?mmHg were randomized (1:1) to receive VAL80/HCTZ12.5?mg (n?= 429) or VAL80?mg (n?= 435) for 8?weeks.

Main outcome measures: The efficacy variable was changed from baseline to endpoint in trough MSDBP. The secondary efficacy variables were changed in mean sitting systolic blood pressure (MSSBP), response rate, and control rate.

Results: Significant reductions in MSDBP and MSSBP from baseline to endpoint were observed in both groups. There were significantly greater reductions in MSDBP (8.4?mmHg vs. 6.2?mmHg) and MSSBP (10.2?mmHg vs. 6.7?mmHg), higher response (64.2% vs. 52.5%) and control rates (53.9% vs. 40.9%) in the VAL80/HCTZ12.5 group as compared with the VAL80 group at endpoint (?p?<?0.001). VAL80/HCTZ12.5 was equally effective in both age subgroups (≥?65 and <?65?years) and was well tolerated. There were no deaths and the two serious adverse events reported were unrelated to study medication.

Conclusion: In Chinese patients with mild-to-moderate essential hypertension not adequately controlled by VAL 80?mg alone, VAL80/HCTZ12.5?mg combination was well tolerated and showed additional BP reduction. The limitations of this study were the inability to include an HCTZ arm as a control group and the short trial duration.

Trial registration: NCT00250562.     

Effect of antihypertensive treatment with valsartan or atenolol on sexual activity and plasma testosterone in hypertensive men

OBJECTIVE: To compare the effects of valsartan and atenolol on sexual activity and plasma testosterone in newly diagnosed, previously untreated, essential hypertensive male subjects. METHODS: One hundred and ten hypertensive men, aged 40-49 years, homogeneous for marital status and without any previous sexual dysfunction were randomly treated with valsartan 80 mg daily (o.d.) or atenolol 50 mg o.d. for 16 weeks according to a double-blind, parallel-arm study design. After 8 weeks the dose was doubled in the non-responders (diastolic blood pressure > 90 mmHg). Clinical evaluation was performed after 8 weeks and 16 weeks of treatment and included blood pressure and plasma testosterone measurements and the compilation of a questionnaire about sexual activity (sexual intercourse episodes/month). RESULTS: Despite similar blood pressure lowering, atenolol significantly reduced sexual activity (from 6.0 sexual intercourse episodes/month to 4.2 sexual intercourse episodes/month, P < 0.01 vs placebo), whereas valsartan increased it, although not significantly (from 5.8 sexual intercourse episodes/month to 7.4 sexual intercourse episodes/month, P = 0.058), compared with placebo, but significantly compared with the atenolol group ( P < 0.05). Testosterone was reduced by atenolol (from 18.2 nmol/l to 13.8 nmol/l, P < 0.01 vs baseline) but was not affected by valsartan (from 17.6 nmol/l to 18.3 nmol/l). CONCLUSIONS: These results suggest that atenolol induces a worsening of sexual activity and a reduction of testosterone, whereas valsartan does not worsen sexual activity and does not change testosterone levels.     

缬沙坦分散片的研制

目的制备缬沙坦分散片并对其相关性能进行考察。方法采用L9(34)正交试验设计法,以综合评分法筛选出最佳处方;采用紫外分光光度法测定产品45min的累积溶出度。结果优化后的处方制得的分散片外观光洁,在1min内完全崩解,20min溶出度可达95%以上,各项指标均符合药典规定。结论优化所得处方合理,制备工艺简单,产品性能良好。     

Comparison of the antihypertensive effects of celiprolol and acebutolol

Summary The antihypertensive effects of the new cardioselective beta-blocker celiprolol and acebutolol have been compared. Thirty patients with arterial hypertension WHO Grade I–II were treated in a double-blind fashion with celiprolol or acebutolol. Before starting the treatment and on Days 15 and 29, before the morning dose, blood samples were taken for measurement of the plasma level of celiprolol. At the same times physical examinations, and clinical and urine chemistry analyses were performed.At the 99% probability level both drugs had significantly lowered the systolic and diastolic blood pressures to normal values at the end of the second and fourth weeks. There was no significant difference between their antihypertensive efficacy. The decrease in diastolic blood pressure at the end of the second week was significantly correlated with the reciprocal of the plasma celiprolol concentration at steady-state at the end of the dosage interval.This paper was presented in part at the 5th Symposium on Biopharmaceutics and Pharmacokinetics, Piestany, Czechoslovakia, May 19–23, 1986, and at the 1st International Symposium on Clinical Pharmacology, Sofia, Bulgaria, September 19–21, 1986     

Renal effects of antihypertensive drugs

Antihypertensive drugs have disparate effects on renal haemodynamics, tubular function, plasma electrolytes, and hormonal responses. Calcium entry blockers and angiotensin-converting enzyme (ACE) inhibitors are unique in that they may increase glomerular filtration rate (GFR) and renal blood flow in patients with hypertension. Both classes of drugs are distinctive in that they prevent salt retention because of their inhibitory effect on tubular sodium reabsorption. In addition to these attributes, which are desirable in terms of lowering systemic blood pressure, these 2 classes of drugs exert important intrarenal effects which may participate in limiting the progression of renal disease. ACE inhibitors have been shown to protect against the development of glomerulosclerosis in various experimental models of renal insufficiency. Importantly, there is emerging evidence from human studies supporting a distinctive beneficial effect of these agents on renal function in patients with hypertension, mild chronic renal insufficiency and diabetes mellitus. Calcium entry blockers have also been shown to exert some beneficial effect in limiting the progression of experimental kidney disease but neither an improvement in glomerular sclerosis nor a decrease in proteinuria have been clearly documented. At present ACE inhibitors appear the most attractive agents in terms of arresting the progression of renal disease. Acute deterioration in renal function may occur following the administration of ACE inhibitors, calcium entry blockers, and beta-blockers. This complication should be considered in every patient on antihypertensive therapy who suffers an unexplained deterioration in renal function. In particular, the sudden deterioration in renal function following initiation of therapy with an ACE inhibitor is a clue to the possible presence of bilateral renal artery stenosis or stenosis of a solitary functioning kidney. Renal damage may also occur in patients with unilateral renal artery stenosis even though total (2-kidney) GFR may not be appreciably reduced. In this setting, a captopril renal scan with hippuran and diethylenetriamine pentaacetic acid (DTPA) provides physiological information regarding the renal blood flow and GFR of each kidney. In patients with unilateral renal artery stenosis the impact of ACE inhibitor therapy on GFR may be discerned by the use of the DTPA scan, which may demonstrate a reduction in GFR in the stenotic kidney that is not apparent by evaluation of total kidney GFR. This suggests that despite adequate control of systemic blood pressure and unchanged plasma creatinine progressive kidney damage in the stenotic kidney ensues.