肾性高血压的诊治

肾性高血压指原发性肾实质或肾血管病变所导致的高血压,占继发性高血压首位,其恶性程度通常比原发性高血压高,更易导致眼底及心脑血管等靶器官的损害,肾脏疾病是顽固性高血压的一个常见而未得到足够重视的病因。长期肾动脉高压造成肾小球内高压、高灌注、高滤     

肾性高血压的诊治

肾性高血压指原发性肾实质或肾血管病变所导致的高血压,占继发性高血压首位,其恶性程度通常比原发性高血压高,更易导致眼底及心脑血管等靶器官的损害,肾脏疾病是顽固性高血压的一个常见而未得到足够重视的病因.长期肾动脉高压造成肾小球内高压、高灌注、高滤过,从而加速肾小球动脉硬化、纤维化,进一步损害肾功能.可见,肾脏既是高血压的病因所在,又是受害者,积极控制高血压对肾功能的保护至关重要.     

苯磺酸左旋氨氯地平对原发性高血压患者血浆内皮素及肾功能的影响

高血压是促进动脉硬化发生及发展的重要危险因子。长期高血压可引起全身动脉病变，包括血管管壁增厚、胶原增生、弹性纤维减少或撕裂，甚至管壁钙化，从而导致血管内皮功能异常。同时高血压还可以导致心、脑、肾等靶器官损害。肾脏是高血压最常累及的重要脏器之一。研究发现血压波动与早期肾脏损害有关。本研究通过检测高血压患者血浆内皮素（ET）、肾小球滤过率（GFR）等指标评价长效二氢吡啶类钙通道阻滞剂（CCB）苯磺酸左旋氨氯地平对高血压患者血管内皮功能及早期肾功能的保护作用。     

左旋氨氯地平对高血压疾病中靶器官保护作用的研究进展

目的:介绍左旋氨氯地平对高血压疾病中靶器官保护作用的研究状况。方法:综述文献,分析左旋氨氯地平对左心室肥厚及其舒张功能、肾脏功能、胰岛素抵抗、血管内皮功能、颈动脉粥样硬化病变的改善作用。结果与结论:左旋氨氯地平减退左心室肥厚可能与其增加钠盐排泄抵消了肾上腺素能活性有关;其能阻滞细胞膜的钙通道,使进入细胞内的钙离子减少,有利于心肌的去收缩活动,从而逆转心室舒张功能不全;其能持久扩张肾小球入球小动脉,使肾血流量和肾小球滤过率升高,改善肾脏缺血,阻止肾血管和肾小球结构和功能的紊乱;其可扩张血管平滑肌,增加骨骼肌血流量,提高机体胰岛素受体前水平对胰岛素的敏感性;其具有的抗氧化、减轻血管平滑肌细胞增生、抗血小板聚集作用,可逆转颈动脉内-中膜增厚和改善内皮功能。左旋氨氯地平具有多种靶器官的保护作用,有良好的研究和应用前景。     

尼卡地平和硝酸甘油在高血压急症治疗中的应用

高血压急症是指高血压患者血压在短时间内急骤升高,同时伴有心、脑、肾、视网膜等重要靶器官功能损害的一种严重危及生命的临床综合征,其发生率占高血压患者的5％左右.高血压急症常引起靶器官的功能严重障碍,甚至衰竭.快速诊断并及早开始治疗是避免靶器官损害的关键[1]. 目前可用于急诊快速降压的药物有硝普钠、硝酸甘油、酚妥拉明、尼卡地平及乌拉地尔等.其中硝酸甘油因其相对低廉的价格及低血压风险较小,成为国内大部分急诊静脉降压药物的首选.     

高血压急症的分类及处理

高血压急症(Hypertensiveemergencies,HE)是指原发性或继发性高血压患者在疾病的发展过程中,或在某些诱因作用下,出现血压显著地或急剧升高(通常舒张压>16kPa(120mmHg)),常伴有急性或进行性的心、脑、肾、视网膜等重要靶器官功能损害甚至衰竭。高血压急症是由血压急剧升高引起的,对靶器官功能及生命预期性威胁,必须紧急或及时处理。     

原发性高血压病患者血糖水平与蛋白尿的相关性

<正>高血压病患者合并糖代谢紊乱可以引起严重的心、脑、肾等靶器官损害。肾脏是高血压和糖尿病最常累及的靶器官。尿微量白蛋白排泌量对判断肾脏早期损害有重要价值。本文旨在探讨高血压病患者糖代谢异常与尿微量白蛋白排泌量的相关性,以指导临床治疗。     

氨氯地平治疗老年高血压患者效果的临床观察

<正>高血压病是人群中的一种常见病和多发病,多见于老年人群,易损害其心脑肾血管等靶器官,造成相应并发症的发生。随着我国老龄化程度的逐渐加剧,老年高血压的患病率呈逐年上升趋势,是我国亟待解决的一个严重的公共卫生问题。随着年龄的增长,老年人生理机能的退化,致使老年高血压患者靶器官损害的程度比中青年人更为严重,罹患心脑血管和肾脏等慢性疾病的几率明显提高,由此所导致的     

高血压性肾损害

肾脏是高血压的靶器官之一,长期高血压可引起肾硬化。高血压病的类型决定了肾硬化的病理。原发性高血压缓进型可导致良性肾硬化症,恶性肾硬化症是原发性高血压急进型最显著的并发症;当临床上缓进型在病程的某一阶段转变为急进型时,良性肾硬化症亦发展为恶性肾硬化症(约占1～8%)。一、良性肾硬化症血压长期升高,肾脏的细小动脉发生硬化,称肾小动脉肾硬化症;由于本症进程相当缓慢,多数患者不会出现肾功能衰竭,所以又名良性肾硬化症。小动脉内膜下类脂质沉积和透明样变是本症的主要病理变化。透明物质主要由糖蛋白和胶原基质组成,由于这些物质的沉积,造成血管壁增厚,弹力纤维减     

厄贝沙坦对老年高血压患者血流变学和肾结构的影响

高血压病可导致心、脑、肾等靶器官损害，血压的水平与致死性、非致死性心血管疾病的病死率呈相关性。另外，高血压与肾功能的减退和肾衰竭的发生也相关。因此，如何更好地控制血压并保护血管和肾脏，成为临床关注的问题。本文通过对老年高血压患者使用厄贝沙坦药物干预，观察患者血液流变学指标、肾血流、。肾血管结构的改变，现将结果报道如下：     

Vascular endothelin in hypertension

Endothelins are powerful vasoconstrictor peptides that also play numerous other functions in many different organs. Endothelin-1 (ET-1) is the most abundant and important of this family of peptides in blood vessels. Production of ET-1 is increased in the endothelium and the kidney in salt-dependent models of hypertension (e.g.: DOCA-salt rats and Dahl salt-sensitive rats, in salt-loaded SHR-SP, in angiotensin II-infused and in diabetic rats). ET-1 elicits an inflammatory response by increasing oxidant stress in the vascular wall, which induces vascular remodeling and endothelial dysfunction found in the hypertensive models that exhibit an endothelin-mediated component. Endothelin receptor antagonism reduces blood pressure and vascular hypertrophic remodeling present in these hypertensive models. Patients with stage 2 hypertension have enhanced vascular expression of ET-1. Endothelin receptor antagonists lower blood pressure in hypertensive patients. They could become therapeutic agents for prevention of target organ damage in hypertension and in type 2 diabetes, chronic renal failure and congestive heart failure. Side effects of endothelin receptor blockers have prevented up to the present their development for these indications. New endothelin antagonists devoid of these side effects, or alternatively inhibitors of the endothelin converting enzymes that generate ET-1 may in the future become available to block the endothelin system. However, to date endothelin antagonists have been approved only for the treatment of primary pulmonary hypertension, a rapidly fatal condition in which the endothelin system plays an important role and endothelin antagonists exert favorable effects.     

新一代血管紧张素转换酶抑制剂——福辛普利

福辛普利为第三代含膦酸基的血管紧张素转换酶抑制剂(ACEI),通过特异性抑制周围血管和组织的血管紧张素转换酶的途径阻断血管紧张素Ⅱ的合成,同时抑制激太酶,使缓激肽降解减少,促进血管内皮释放舒血管物质,降压起效缓慢,逐渐增强,在四周时达最大效应,限制钠盐摄入或联合使用利尿剂可使起效迅速和作用增强.福辛普利具有改善胰岛素抵...     

Matrix metalloproteinases and small artery remodeling

Inward eutrophic remodeling is a common structural change found in small resistance arteries that has been associated with an increased risk for life threatening cardiovascular events, the number one cause of death in industrialized societies. Because inward eutrophic remodeling is the most prevalent small artery structural change found in hypertension, hypertensive animals are the most common in vivo models used to study this particular remodeling process. In vitro, the isolated artery, pressure myograph has also been used as a model to study the mechanisms responsible for the development of small artery remodeling. Compelling recent evidence indicates that the matrix metalloproteinases (MMPs), a family of endopeptidases whose primary function is the cleavage and degradation of extracellular matrix components, are involved in vasoconstriction and the pathogenesis of hypertension. In this review we provide an overview of the known and potential roles that MMPs have on vascular remodeling, paying particular attention to their role on the inward eutrophic remodeling process of small resistance arteries that occurs in hypertension.     

Structural alterations in small resistance arteries in obesity

In cardiovascular and metabolic diseases, small resistance arteries may show the presence of structural alterations. In particular, in essential hypertension, an increased media-to-lumen ratio of subcutaneous small arteries with no change in the total amount of vascular wall tissue (eutrophic remodelling) has already been described several years ago. Similar alterations have been demonstrated also in patients with diabetes mellitus and obesity; in this case, however, a more evident contribution of vascular smooth muscle cell growth (hypertrophic remodelling) is present. This review addresses the effects of obesity on small resistance artery structure. Similar to diabetic patients, obese patients show an increased media-to-lumen ratio of subcutaneous small arteries, which appears associated with hypertrophic remodelling, as demonstrated by an increase in media cross-sectional area. Endothelial dysfunction evaluated as vasodilator response to acetylcholine has also been observed. Several studies have shown that increased media-to-lumen ratio of subcutaneous small resistance arteries possesses a prognostic significance in relation to cardiovascular outcome. Appropriate antihypertensive treatment may improve microvascular alterations both in essential hypertension and in type 2 diabetes mellitus. In obesity, a pronounced weight loss may improve microvascular structure. However, further studies are needed to elucidate the effects of other pharmacological and non-pharmacological interventions in obesity.     

Hypertension in the elderly: an evidence-based review

The progressive ageing of world population, and the increasing prevalence hypertension in elderly people are leading to the consideration that hypertension in the elderly is one of the main topic in hypertension treatment. Multiple mechanisms, including stiffening of large arteries, endothelial dysfunction, cardiac remodeling, autonomic dysregulation, renal aspects, contribute to the great prevalence of hypertension in the elderly and to increased cardiovascular morbidity and mortality. Treatment of hypertension can hardly put back older patients in a low risk category, especially if target organ damage is present. Nevertheless, blood pressure control can successfully prevent stroke, cognitive decline, coronary heart disease and heart failure, and reduce mortality in the elderly, and even in patients > 80 years, as recently demonstrated. Blood pressure should be lowered below 140/90 mmHg also in older patients. However the HYVET study suggests that a goal of 150/90 mmHg can be reasonable in patients aged 80 years or more. Drug treatment should be titrated with particular caution to adverse responses and excessive blood pressure lowering.     

转化生长因子β1与高血压及其靶器官损害的研究进展

原发性高血压病是一种遗传和环境因素综合作用,引起的心血管系统,体液调节功能失调而致的血管平滑肌、心肌及细胞外基质（extracellular matrix,ECM）增生性疾病,常影响重要脏器如心、脑、肾的结构和功能。转化生长因子β1（TGF-β1）是一种调节细胞生长和分化及细胞外基质生成的多功能细胞因子。近来研究表明,TGF-β1及其介导的信号转导在高血压的发生、发展及转归中起着重要作用。现就TGF-β1在高血压及其靶器官的损害中作用的研究进展作一综述。     

Intra- and extrarenal arteries exhibit different profiles of contractile responses in high glucose conditions

Background and purpose:

The renal artery (RA) has been extensively investigated for the assessment of renal vascular function/dysfunction; however, few studies have focused on the intrarenal vasculature.

Experimental approach:

We devised a microvascular force measurement system, which allowed us to measure contractions of interlobar arteries (ILA), isolated from within the mouse kidney and prepared without endothelium.

Key results:

KCl (50 mM) induced similar force development in the aorta and RA but responses in the ILA were about 50% lower. Treatment of RA with 10 μM phenylephrine (PE), 10 nM U46619 (thromboxane A₂ analogue) or 10 μM prostaglandin F_2α elicited a response greater than 150% of that induced by KCl. In ILA, 10 nM U46619 elicited a response that was 130% of the KCl-induced response; however, other agonists induced levels similar to that induced by KCl. High glucose conditions (22.2 mM glucose) significantly enhanced responses in RA and ILA to PE or U46619 stimulation. This enhancement was suppressed by rottlerin, a calcium-independent PKC inhibitor, indicating that glucose-dependent, enhanced small vessel contractility in the kidney was linked to the activation of calcium-independent PKC.

Conclusion and implications:

Extra- and intrarenal arteries exhibit different profiles of agonist-induced contractions. In ILA, only U46619 enhanced small vessel contractility in the kidney, which might lead to renal dysfunction and nephropathy through reduced intrarenal blood flow rate. A model has been established, which will allow the assessment of contractile responses of intrarenal arteries from murine models of renal disease, including type 2 diabetes.     

氯沙坦对肾性高血压大鼠肠系膜动脉血管重构的影响

目的:观察氯沙坦对两肾一夹高血压大鼠(2K1C)肠系膜动脉血管重构的影响.方法:建立2K1C高血压大鼠模型.夹尾法测定大鼠血压.在实验结束时,使用磷酸盐缓冲溶液对大鼠进行灌注,再用4％多聚甲醛在体灌注,取肠系膜动脉,10％福尔马林保存进行形态学分析.结果:肾动脉狭窄大鼠较假手术大鼠血压明显升高(P＜0.01),在10周末给予氯沙坦干预,能剂量依赖性地显著降低血压(P＜0.01).给予氯沙坦干预4周,大鼠肠系膜动脉血管重构参数,即中膜面积/管腔面积比值和中膜厚度/管腔直径比值显著降低.结论:氯沙坦能够逆转肾性高血压大鼠肠系膜动脉血管重构.     

Molecular mechanisms for vascular injury in the metabolic syndrome

The metabolic syndrome is strongly associated with insulin resistance and has been recognized as a cluster of risk factors for cardiovascular diseases such as visceral obesity, hypertension, diabetes and dyslipidemia. Recently, insulin resistance in the absence of overt diabetes or the metabolic syndrome itself has been shown to be associated with endothelial dysfunction, one of the initial steps in the process of atherosclerosis. In the present article we review the molecular mechanisms by which the metabolic syndrome causes endothelial dysfunction and subsequently promotes atherosclerosis. We also discuss promising therapeutic strategies that specifically target the mechanisms responsible for vascular alterations in the metabolic syndrome.