槲寄生、钩藤、杜仲降压作用及急性毒性的实验研究

目的研究槲寄生、钩藤、杜仲的水提液及其混合液的降血压作用及急性毒性反应.方法用肾动脉结扎法制备高血压大鼠模型,灌胃给予中药水提液,考察降血压作用.用小鼠灌胃考察急性毒性.结果槲寄生杜仲混合水提液、钩藤杜仲混合水提液、槲寄生钩藤杜仲混合水提液均能降低高血压大鼠的血压,槲寄生杜仲混合水提液和槲寄生钩藤杜仲混合水提液的效果更为明显,能将大鼠血压降到正常水平,并维持稳定.结论槲寄生、钩藤、杜仲三味中药不同配伍有较好的降压作用,且三种混合水提液对小鼠按照最大耐受量灌胃,未见急性毒性反应.     

天麻钩藤饮对腹主动脉狭窄-高盐型高血压大鼠血压等因素的影响

目的 观察天麻钩藤饮对腹主动脉狭窄-高盐型高血压大鼠血压等因素的影响.方法 将25只SD大鼠随机分为假手术组、实验性高血压组、实验性高血压天麻钩藤饮灌胃组.用手术和高盐饲养的方法制成腹主动脉狭窄-高盐摄入型高血压大鼠,在制备高血压病理模型的同时,用药组每天用天麻钩藤饮灌胃,观察30 d后对大鼠血压、心率及心指数的影响.结果 30 d后,高血压病理模型未用药组与假手术组比较血压明显升高,心率加快,心指数增加,均有统计学意义(P<0.05);高血压病理模型用药组与未用药组比较血压减低,心率减慢,心指数减少,均有统计学意义(P<0.05).结论 天麻钩藤饮可降低腹主动脉狭窄-高盐型高血压大鼠的血压、心率及心指数.     

平肝潜阳法对自发性高血压大鼠血管结构和功能的影响研究

目的本课题旨在探讨平肝潜阳法对白发性高血压大鼠（SHR）的血压及心、肾血管的组织形态学改变,抗氧化血清酶一氧化氮及一氧化氮合酶的活性变化。血管内皮型一氧化氮合酶蛋白表达的影响,以期进一步阐明平肝潜阳法对血管结构和功能的作用机制,为中医药防治高血压提供实验依据。方法选用12周龄自发性高血压雄性大鼠45只,随机分为5组,即天麻钩藤饮组（A组）、天麻钩藤饮去石决明组（B组）、硝苯地平组（C组）、石决明组（D组）、生理盐水对照组（E组）。治疗4W后,测量收缩压;测定血清游离钙浓度;用HE染色观察心肾血管组织切片;使用紫外分光光度计测定血清NO、NOS指标的活力变化;使用SABC染色法检测心脏血管和肾血管eNOS蛋白表达并用全自动图像分析系统进行结果分析。结果①天麻钩藤饮组用药4W后与实验前SHR血压下降最明显（P〈0．01）,②用药前后天麻钩藤饮组和硝苯地平组血清游离钙浓度改变没有统计学意义（P〉0．05）。③形态学观察结果显示：天麻钩藤饮组能改善高血压并发心、肾血管的病理损坏,促进损坏组织修复较其它各组明显。④天麻钩藤饮组和天麻钩藤饮去石决明组NO、NOS的含量增高与生理盐水对照组比较有统计学意义（P〈0．05）,以天麻钩藤饮组改变最明显（P〈0．01）。⑤天麻钩藤饮组和天麻钩藤饮去石决明组的心脏和肾脏血管eNOS蛋白表达灰度值与生理盐水组比较有统计学意义（P〈0．05）,以天麻钩藤饮组改变最明显（P〈0．01）。结论①天麻钩藤饮和硝苯地平能够抑制早期的高血压,天麻钩藤饮长期降压效果优于硝苯地平。②天麻钩藤饮有明显改善心肾血管形态,抑制血管平滑肌细胞的增殖,降低血管紧张度的作用。③天麻钩藤饮的扩张血管,抑制血小板黏附聚集作用明显优与钙拮抗剂硝苯地平和石决明。     

钩藤总碱与天麻素联用对自发性高血压大鼠血压和血压变异性的影响

背景钩藤和天麻是治疗高血压的传统中药,常联合应用。目的研究钩藤、天麻的活性成分钩藤总碱及天麻素抗高血压和改善血压变异性的协同作用。方法 60只自发性高血压大鼠随机分为11组,分别是:对照组、钩藤总碱4组(25、50、100、200mg/kg)、天麻素3组(8、80、800mg/kg)、钩藤总碱+天麻素3组[(50+8)、(50+80)、(50+800)mg/kg],腹腔给药。采用清醒自由活动大鼠血压测定系统监测给药前后大鼠的血压和血压变异性。用两因素多水平析因设计、概率和法和q检验方法评价钩藤总碱和天麻素降压以及改善血压变异性的协同作用。结果在25～200mg/kg剂量范围内,钩藤总碱给药量与血压降低幅度有量效关系。其中,200mg/kg剂量组给药前后收缩压分别为(182±16)和(142±12)mmHg,舒张压分别为(133±21)和(100±19)mmHg,给药前后血压平均值的差异有统计学意义(P<0.01)。天麻素单独注射剂量达到800mg/kg也没有降低自发性高血压大鼠的血压。而钩藤总碱+天麻素组[(50+8)、(50+80)、(50+800)mg/kg]有降压作用,钩藤总碱和天麻素联用具有协同降压作用,对血压变异性没有不良影响。结论钩藤总碱具有确切的降压作用,但对血压变异性没有影响。天麻素本身不降低血压,但与钩藤总碱联用具有协同降压作用。     

天麻钩藤饮联合针刺对自发性高血压大鼠的降压作用及机制研究

目的研究天麻钩藤饮联合针刺对于自发性高血压大鼠(SHR)的降压效果及作用机制。方法使用随机数字表法将40只SHR分为4组:针刺组、天麻钩藤饮组、针刺+天麻钩藤饮组、模型组,每组10只。检测治疗前后各组大鼠的血压、神经肽Y(NPY)和内皮素-1(ET-1)水平。结果①血压变化方面:治疗2周、治疗4周时,针刺+天麻钩藤饮组较针刺组、天麻钩藤饮组血压下降更明显,差异均有统计学意义(P<0.05);治疗2周时,天麻钩藤饮组、针刺+天麻钩藤饮组较模型组血压下降更明显,差异均有统计学意义(P<0.05);治疗4周时,针刺组、天麻钩藤饮组、针刺+天麻钩藤饮组较模型组血压下降更明显,差异均有统计学意义(P<0.05)。②NPY及ET-1变化方面:针刺+天麻钩藤饮组NPY、ET-1水平较针刺组、天麻钩藤饮组降低更明显,差异均有统计学意义(P<0.05);针刺组、天麻钩藤饮组、针刺+天麻钩藤饮组NPY水平较模型组降低更明显,差异均有统计学意义(P<0.05);天麻钩藤饮组、针刺+天麻钩藤饮组ET-1水平较模型组降低更明显,差异均有统计学意义(P<0.05)。结论天麻钩藤饮联合针刺对于高血压的降压作用比单独应用针刺或天麻钩藤饮更加显著,两者联合应用可能存在协同效应,这种效应的发挥可能与血清NPY和ET-1的降低有关。     

天麻多糖的降血压作用

目的从天麻中提取出天麻多糖(PGB),研究PGB对高血压模型大鼠的降血压作用。方法水提醇沉法提取出天麻粗多糖,DEAE-52纤维素柱分离纯化得PGB。用两肾一夹(2K1C)方法制作高血压模型(RHR)大鼠,以卡托普利(10mg/kg·d)为阳性对照组,以服用自来水为阴性对照组,以天麻多糖低、中、高3个浓度(50、100、200mg/kg·d)给药30d后测定大鼠心率与血压的变化,尿量的变化,以及血清中一氧化氮(NO)、血浆内皮素(ET)和血管紧张素Ⅱ(AngⅡ)水平的变化。结果天麻多糖PGB能明显降低RHR大鼠的收缩压和舒张压(P<0·05),尤其是中、高剂量组(P<0·01),并且在剂量范围内呈剂量依赖性;对大鼠心率及尿量没有明显作用;血清NO含量(51·9±9·8vs对照组40·7±10·2)μmol/L,血浆ET含量下降(164±25vs对照组209±10)μmol/L,AngⅡ含量下降(247±20vs对照组310±37)μmol/L,P值均<0·01。结论天麻多糖对RHR大鼠具有良好的降压作用,其作用机制与促进内源性舒血管物质的生成及抑制内源性缩血管物质的释放,最终恢复二者拮抗效应的平衡有关。     

天麻钩藤饮正交方对肝阳上亢证高血压大鼠血管内膜的影响

目的 观察天麻钩藤饮正交配方对肝阳上亢证高血压大鼠血管内膜和中膜的影响.方法 将90只清洁级SD健康大鼠,雌雄各半,随机分为正常对照组(A组)、模型组(B组)、卡托普利组(C组)、天麻钩藤饮组(D组)、正交Ⅰ方组(E组)、正交Ⅱ方组(F组),每组15只.后5组采用钳夹左肾动脉加灌附子汤法制备肝阳上亢证高血压大鼠模型.造模6周后,C组、D组、E组、F组灌胃给药2周,观察各给药组血管内膜和中膜病理形态学改变,并测量其左心室重量指数.结果 各给药组均能降低模型大鼠血压,C组优于D组、F组(P<0.01),但与E组比较无统计学意义(P>0.05).各给药组均能减轻血管中膜病变,并能减少左室重量指数.结论 天麻钩藤饮及其正交配方均有保护靶器官的作用,但正交1方能提高降压效应.     

天麻多糖的降血压作用

目的从天麻中提取出天麻多糖(PGB),研究PGB对高血压模型大鼠的降血压作用.方法水提醇沉法提取出天麻粗多糖,DEAE-52纤维素柱分离纯化得PGB.用两肾一夹(2K1C)方法制作高血压模型(RHR)大鼠,以卡托普利(10 mg/kg·d)为阳性对照组,以服用自来水为阴性对照组,以天麻多糖低、中、高3个浓度(50、100、200 mg/kg·d)给药30 d后测定大鼠心率与血压的变化,尿量的变化,以及血清中一氧化氮(NO)、血浆内皮素(ET)和血管紧张素Ⅱ(Ang Ⅱ)水平的变化.结果天麻多糖PGB能明显降低RHR大鼠的收缩压和舒张压(P＜0.05),尤其是中、高剂量组(P＜0.01),并且在剂量范围内呈剂量依赖性;对大鼠心率及尿量没有明显作用;血清NO含量(51.9±9.8 vs 对照组40.7±10.2)μmol/L,血浆ET含量下降(164±25 vs 对照组209±10)μmol/L,Ang Ⅱ含量下降(247±20 vs对照组310±37)μmol/L,P值均＜0.01.结论天麻多糖对RHR大鼠具有良好的降压作用,其作用机制与促进内源性舒血管物质的生成及抑制内源性缩血管物质的释放,最终恢复二者拮抗效应的平衡有关.     

血府逐瘀汤、天麻钩藤饮、温胆汤对自发性高血压大鼠心肌组织 MAPK 信号通路的影响

目的：观察血府逐瘀汤、天麻钩藤饮、温胆汤对自发性高血压大鼠心肌组织丝裂原活化蛋白激酶信号通路的影响。方法将60只16周龄自发性高血压大鼠随机分为阳性对照组、蛋白酶体抑制剂（ MG-132）组、血府逐瘀汤组、温胆汤组、天麻钩藤饮组各12只,另取12只正常血压大鼠作为阴性对照组。 MG-132组腹腔注射MG-132,血府逐瘀汤组、天麻钩藤饮组、温胆汤组分别给予相应的药物灌胃,阳性对照组、阴性对照组给予等量生理盐水灌胃。连续用药8周后断头处死,取大鼠心脏,采用LiquiChip液相蛋白芯片系统检测各组大鼠心肌组织c-Jun氨基末端激酶（JNK）、p38丝裂原活化蛋白激酶（p38MAPK）、细胞外信号调节激酶5（ERK5）。结果与阴性对照组比较,阳性对照组JNK水平升高,阳性对照组、天麻钩藤饮组、温胆汤组、血府逐瘀汤组、MG132组p38MAPK及ERK5水平升高（P均＜0．01）;与阳性对照组比较,天麻钩藤饮组、温胆汤组、血府逐瘀汤组、MG132组p38MAPK及ERK5水平降低（P均＜0．01）;与MG132组比较,天麻钩藤饮组、温胆汤组、血府逐瘀汤组p38MAPK水平升高（P均＜0．01）;与天麻钩藤饮组、温胆汤组比较,血府逐瘀汤组p38MAPK及ERK5水平降低（P均＜0．05）。结论血府逐瘀汤、天麻钩藤饮、温胆汤可抑制大鼠心肌组织JNK、p38 MAPK、ERK5的表达,血府逐瘀汤较另外两种方剂抑制作用更为明显。     

血府逐瘀汤、温胆汤、天麻钩藤饮对SHR大鼠心肌组织TNF-α、IFN-γ、G-CSF、MCP-1表达的影响

目的观察血府逐瘀汤、温胆汤、天麻钩藤饮对自发性高血压(SHR)大鼠心肌组织中TNF-α、IFN-γ、粒细胞集落刺激因子(G-CSF)、单核细胞趋化蛋白-1(MCP-1)等炎性细胞因子表达的影响。方法将50只16周龄SHR大鼠随机分为5组,SHR对照组、卡托普利组、天麻钩藤饮组、温胆汤组和血府逐瘀汤组各10只;另取10只血压正常的WKY大鼠作为正常对照组。卡托普利组、天麻钩藤饮组、温胆汤组和血府逐瘀汤组分别给予相应的药物灌胃,SHR对照组、正常对照组给予等量生理盐水灌胃,均2次/d,连续灌胃8周。之后断头处死各组大鼠,取其心脏,采用LiquiChip液相蛋白芯片系统检测大鼠心肌组织TNF-α、IFN-γ、G-CSF、MCP-1等炎性细胞因子。结果用药8周后,天麻钩藤饮组、血府逐瘀汤组、温胆汤组大鼠心肌组织TNF-α、G-CSF、MCP-1等炎性细胞因子的表达水平明显降低,IFN-γ的表达升高,与SHR对照组、正常对照组大鼠用药后相比,P均<0.01;血府逐瘀汤组与天麻钩藤饮和温胆汤组相比,P均<0.05。结论血府逐瘀汤、温胆汤、天麻钩藤饮有一定的抗心肌纤维化作用,其机制可能与抑制大鼠心肌组织中TNF-α、G-CSF、MCP-1的表达和提高IFN-γ的表达有关。     

陈可冀辨治高血压病医案的数据挖掘分析

目的挖掘与总结名专家陈可冀老师临床辨治高血压病的学术思想和诊疗规律。方法125例诊断为高血压病经陈可冀老师治疗的病人,将其初诊数据录入数据库,各种名词标准化,利用SQLServer工具对病人的症状、中医诊断、治则、用方、用药等进行统计分析。结果125例高血压病病人出现证候多为阴虚阳亢证、肝阳上亢证、痰瘀互结证等。所处方剂多以天麻钩藤饮、清眩降压汤、栝蒌薤白半夏汤、血府逐瘀汤等化裁。用药次数最多的依次是钩藤、天麻、菊花等。结论高血压病为虚实夹杂的证候,阴虚阳亢证最多见,实象反映为肝阳上亢、瘀血和痰浊。陈可冀老师善于用清眩降压汤治疗高血压病。数据挖掘结果客观反映了陈可冀老师治疗高血压病的临床思路与经验。     

高血压伴肾功能不全57例临床研究

目前,全球由于糖尿病、高血压或其他疾病造成肾脏损害而进入终末期肾病的人数呈上升趋势[1]。高血压与肾脏关系十分密切,肾脏既是血压调节的重要器官,同时又是高血压损害的主要靶器官之一,高血压合并肾功能不全在治疗上比单纯高血压病明显复杂。本文对高血压合并肾功能不全的老     

Sind alle Antihypertensiva nephroprotektiv?

Blood pressure, together with proteinuria, represents one of the most important factors in the progression of chronic renal failure (CRF). Antihypertensive therapy is beneficial to slow down the progression of a variety of chronic renal diseases, no matter what the cause. Intraglomerular hypertension, increased glomerular permeability and proteinuria should be identified, since they can be treated to prevent or minimize further glomerular injury.But not all antihypertensive drugs are equally effective to prevent the progression of CRF. Recent large trials indicate that blood pressure lowering obtained by intervention in the renin-angiotensin-aldosterone system (RAAS) has an additive renoprotective effect in diabetic and nondiabetic renal diseases. In nondiabetic patients, the AIPRI and REIN studies support that angiotensin-converting enzyme (ACE) inhibitors have a long-term renoprotective effect. The benefits of ACE inhibitors can be demonstrated even in patients who are not hypertensive. Angiotensin II receptor antagonists are shown to be renoprotective in type 2 diabetics (RENAAL and IDNT). However, whether these renoprotective effects are due to blood pressure reduction or due to the specific pharmacologic RAAS blockade is still a matter of debate. This discussion is still open, because the reduction in blood pressure levels was lower in patients treated with a drug that interferes with the RAAS compared with other antihypertensive regimens. It is concluded that both ACE inhibitors and AT II receptor antagonists are lowering the intraglomerular pressure independent of any change in systemic blood pressure by dilatation of the efferent arteriole of the glomerulus. These additional nonpressure-related effects may protect renal function by their antiproteinuric effect. In addition, beneficial effect of ACE inhibitors are related to reduction of AT II, which has potent proinflammatory effects independent of its hemodynamic influences.Other drugs, such as diuretics, beta blockers, and hydralazine, do not induce efferent dilatation and, therefore, may be less likely to reverse intraglomerular hypertension. For example, hydralazine and nifedipine appear to produce prominent afferent or preglomerular arteriolar dilatation. This will allow more of the systemic pressure to be transmitted to the glomerulus. Therefore, short-acting dihydropyridine calcium channel blockers (CCB) are not recommended. By comparison, long-acting dihydropyridines such as diltiazem and verapamil are less potent vasodilators and may primarily decrease the resistance of the efferent arteriole, similar to the ACE inhibitors. They may have an antiproteinuric activity. Yet, there is lack of large prospective randomized trials.A beta blocker as antihypertensive agent is indicated as second- or third-line drug especially in patients with additional cardiovascular disease. Other antihypertensive drugs can be added as necessary to achieve the treatment goals for arterial hypertension. The use of a diuretic will often be helpful in patients who already have renal insufficiency, since fluid overload is an important cause of hypertension and may also enhance the effectiveness of drugs that interfere with the RAAS. alpha(1)-receptor or sympathetic blockers are further possible drugs for combination antihypertensive therapy.     

Does treatment of non-malignant hypertension reduce the incidence of renal dysfunction? A meta-analysis of 10 randomised, controlled trials

OBJECTIVE: It remains controversial whether non-malignant 'benign' hypertension causes renal dysfunction. The effect of lowering blood pressure on the incidence of renal dysfunction among patients with non-malignant hypertension is not clear. This meta-analysis was conducted to determine whether antihypertensive drug therapy reduces the incidence of renal dysfunction in patients with non-malignant hypertension. METHODS: Randomised, controlled trials of antihypertensive drug therapy of more than 1 year duration that reported renal dysfunction as an outcome were identified through MEDLINE search and literature review. A random effects model was used to obtain summary estimates. RESULTS: Ten trials were identified, involving 26, 521 individuals and 114 000 person-years. All excluded subjects with advanced baseline renal disease. Definition of renal dysfunction outcome varied among trials but within each trial was applied similarly to both treatment and control groups. Drug treatment consisted mostly of diuretics and adrenergic blockers. Overall, treated patients had lower blood pressure and fewer cardiovascular events. There were a total of 317 cases of renal dysfunction. Patients randomised to antihypertensive therapy (or more intensive therapy) did not have a significant reduction in their risk of developing renal dysfunction (relative risk = 0.97; 95% confidence interval (CI) 0.78-1.21; P = 0.77). CONCLUSIONS: Among patients with non-malignant hypertension enrolled in randomised trials, treated patients did not have a lower risk of renal dysfunction. The 95% CI suggests that a 25% or more true protective effect of antihypertensive drugs is unlikely.     

Therapy and prognosis of hypertension in chronic nephritis.

Statistical analysis of the realtion between blood pressure and renal function in 421 patients with CGN, referred to the Second Internal Medicine at Nihon University Hospital, and in 253 Hypertensive patients with CGN by questionaires sent to 29 Medical Universities were investigated. The relationship between survival rate and blood pressure of 84 patients with CGN in Surugadai Nihon University Hospital was also examined. These data show that antihypertensive therapy for CGN with hypertension has an important effect on prognosis. Propranolol was given to 10 hypertensive patients with CGN and hypotensive effect on renal function was observed. Our experience suggests that propranolol may be useful for treating a high renin component in the hypertension with non renal failure, and renal function does not become worse. But in renal failure, propranolol therapy must be used carefully because of inducement to cardiac failure.     

Acute and chronic effects of the angiotensin-converting enzyme inhibitor captopril in severe hypertension

In this study the acute and chronic effect of the converting enzyme inhibitor captopril was investigated in a relatively large number of patients (acute: n = 78, chronic: n = 67) with various forms of severe hypertension, the majority of cases being resistant to a standardized triple therapy (100 mg of hydrochlorothiazide or 80 to 500 mg of furosemide, 320 mg of propranolol and 200 mg of hydralazine). Up to an observed period of 240 minutes, a single oral dose of 25 mg of captopril led to a significant and marked decrease in systolic and diastolic blood pressure. The acute antihypertensive effect of captopril was more pronounced in patients with renovascular than in those with essential or renal parenchymal hypertension. Similar differences among the three groups of patients were also observed during chronic treatment. Over a period of 18 months, patients with renovascular hypertension showed both a more pronounced decrease in mean diastolic blood pressure values and a significantly higher percentage of cases with excellent blood pressure control (diastolic blood pressure 95 mm Hg or less). Under long-term conditions, about 90 percent of all patients required a diuretic and a substantial percentage also needed propranolol as a third drug. Positive correlations between pretreatment plasma renin activity levels and captopril-induced blood pressure reduction were found under acute conditions only. The most frequent side effects were skin manifestations, taste disturbances, dizziness and unproductive cough. Serious adverse effects were rare and included one case of leukopenia and one of the nephrotic syndrome, both being reversible after withdrawal of captopril.Our results demonstrate that captopril is a very potent blood pressure lowering agent in severe hypertension especially in cases of renovascular hypertension. However, currently the potential risk of serious side effects should induce the physician to reserve this drug for those patients with truly resistant hypertension.     

Contribution of Renal Angiotensin Converting Enzyme(ACE) to Blood Pressure Regulation: Possible Role of Brush Border Ace

The role of renal angiotensin converting enzyme(ACE) in blood pressure regulation is not well understood. In our studies, both acute and chronic treatment of hypertensive rats SHR and SHRSP with ACE inhibitors Enalapril and SA446 had a blood pressure lowering effect that coincided with an inhibition of renal cortical and aortic ACE, but not plasma ACE. Further, ACE activities in the renal cortex and aorta were found to increase with aging of the SHRSP, therefore concomitantly with hypertension development. In the kidney, brush border membranes(BBM) contained abundant ACE. We found that the activities of ACE in the renal cortex closely correlated to the activities in isolated BBM, in Wistar Kyoto rats and in the SHRSP. Thus, renal cortical ACE activity and blood pressure correlated in cases of ACE inhibition and hypertension development. Since the ACE activity in the renal cortex appeared to reflect the enzyme activity in BBM, the brush border ACE may have to be taken into account, in view of the relationship between renal ACE, and blood pressure.     

Hypertension management: Special considerations in chronic kidney disease patients

It has been estimated that approximately 11% of the US adult population has chronic kidney disease (CKD), and it has been demonstrated that the prevalence of hypertension rises significantly as renal function declines. Even mild CKD significantly increases mortality risk, and cardiovascular disease remains the main cause of death among these patients. Although CKD patients have generally been excluded from trials testing the effect of lowering blood pressure on cardiovascular outcomes, guidelines suggest lowering blood pressure in hopes of reducing cardiovascular mortality and slowing the progression of renal disease. The preferred antihypertensive agents among these patients are drugs that block the renin-angiotensin system. In most hypertensive CKD patients, however, multiple agents are necessary to reach blood pressure targets. In general, diuretics and calcium channel blockers are added subsequently as adjunctive therapy. Hopefully, with increased recognition of the unique aspects of treating hypertension in this population, end-stage renal disease and cardiovascular morbidity and mortality will be delayed or avoided in the millions of patients with CKD.     

Augmentation of renal blood flow and sodium excretion in hypertensive patients during blood pressure reduction by intravenous administration of the dopamine1 agonist fenoldopam

Activation of dopamine1 (DA1) receptors relaxes vascular smooth muscle, especially in the renal vascular bed. Fenoldopam, the first selective DA1-receptor agonist that can be administered to man, was infused intravenously in 17 patients with essential hypertension (mean blood pressure 152/101 mm Hg). It reduced blood pressure in a dose-dependent fashion at doses between 0.025 and 0.5 microgram/kg/min and the antihypertensive effect was sustained during 2 hr infusions. In 10 patients studied during free-water diuresis, fenoldopam increased renal plasma flow by 42%, glomerular filtration rate by 6%, and sodium excretion by 202%, while lowering mean arterial pressure by 12% (all p less than .05). Similar promotion of sodium excretion was observed during blood pressure reduction in six additional patients studied without water loading. Pronounced enhancement of renal function in spite of blood pressure reduction suggests that fenoldopam might have a special role in the treatment of patients with hypertension and renal impairment.