血管内皮功能障碍与高血压

血管内皮功能障碍与高血压密切相关。一方面血管内皮功能障碍在高血压的发生、发展过程中起重要作用;另一方面高血压本身又加重血管内皮功能障碍,形成恶性循环。现综述血管内皮细胞的生理功能、血管内皮功能障碍的相关因素、血管内皮功能障碍与高血压关系、血管内皮功能检测及血管内皮功能障碍的修复等方面的研究进展。     

血管内皮功能障碍与冠状动脉疾病的关系及防治进展

血管内皮作为循环血液与血管平滑肌之间的中介组织，不仅仅是一层半透性屏障，而且还具有多种重要的生理功能，内皮细胞分泌多种血管活性物质，对维持血管壁张力、血液的流动、管壁的炎症修复和血管的增生具有重要的作用，是功能活跃的代谢组织。内皮细胞损伤会引起内皮功能障碍，与高血压、动脉粥样硬化、心力衰竭等心血管疾病的发生、发展有密切关系。本文就血管内皮功能、血管内皮细胞功能障碍与冠状动脉（冠脉）疾病的关系以及内皮功能保护措施做一综述。     

血管内皮细胞功能障碍与动脉粥样硬化关系的研究进展

血管内皮细胞损伤、内皮功能障碍是动脉粥样硬化的起始环节,其参与动脉粥样硬化的启动和进展过程。内皮功能障碍及形态学损伤引起白细胞-内皮细胞黏附、血管收缩、血小板聚集、氧化应激、平滑肌增殖及血栓形成。内皮细胞功能调节与多种相关因子之间的作用机制是复杂的,本文以内皮细胞功能障碍与动脉粥样硬化关系为切入点,综述血管内皮细胞功能与动脉粥样硬化发生发展的研究进展。     

血管内皮功能障碍及其检测与防治

血管内皮是人体的一个重要组成部分，其功能众多，各种损伤刺激均首先作用于血管内皮细胞，导致功能的降低或紊乱，出现内皮功能障碍，凡是能够引起内皮损伤的各种因素均应看作是导致内皮功能障碍的危险因子包括血脂异常，高血压，糖尿病，炎症与感染，高同型半胱氨酸，吸烟，衰老和绝经，因此，积极寻找内皮功能障碍的早期诊断与防治的方法具有重要意义。     

内皮祖细胞功能异常与高血压心肌肥厚的关系

近年研究发现,高血压左室肥厚的发生、发展与微脉管系统结构及血管内皮细胞功能异常密切相关。一方面血管内皮细胞功能障碍在高血压的发病中起重要作用,而高血压本身又加剧内皮细胞的功能障碍;另一方面,阻力血管和交换血管的再生落后于心肌细胞的增生,受损血管内皮再生减少致使微血管减少,导致重塑的心肌缺血。     

胰岛素抵抗与内皮功能障碍

胰岛素抵抗与动脉粥样硬化的始动环节内皮功能障碍关系密切。胰岛素抵抗时血中游离脂肪酸、非对称性二甲基精氨酸和肿瘤坏死因子а增多,而内皮源性一氧化氮合酶的辅酶四氢叶酸减少,使内皮细胞结构和功能受损从而导致内皮功能障碍。内皮功能障碍与胰岛素抵抗呈恶性循环,两者相互促进,影响动脉粥样硬化的发生发展。     

代谢综合征与血管内皮细胞功能障碍的研究进展

代谢综合征在临床上较为多见,是多种疾病的集合体,其基本病理改变与血管内皮功能障碍密切相关。肥胖、血脂紊乱、高血压、胰岛素抵抗是其特点,其中任何一项都会增加心血管疾病的危险性,同时合并多种异常时,发生心血管疾病的危险性更大,目前已经成为影响人类健康的重大问题。近年来关于代谢综合征和血管内皮功能障碍的研究较多,初步揭示了两者之间的内在关系。本文分别将代谢综合征各组分及中医药与内皮细胞功能障碍的研究进行论述。     

中药调节高血压血管内皮功能的研究进展

高血压病（essential hypertension，EH）是临床常见的心血管疾病之一，而内皮功能障碍在高血压病发生发展中的地位正日益受到重视。本文就高血压与血管内皮功能的关系，中药改善高血压血管内皮功能的实验及临床研究进展做一综述。     

血管内皮功能与冠状动脉粥样硬化关系研究的进展(综述)

自1980年Furchgott等[1]发现血管内皮细胞释放内皮依赖舒张因子EDRF以来,人们开始对血管内皮细胞产生了极大的关注。近年来,随着对内皮细胞功能研究的不断深入,发现血管内皮功能障碍是多种疾病的根源,冠脉粥样硬化与血管内皮功能低下密切相关,研究冠状动脉血管内皮功能障碍的发生、发展规律,对防治冠脉粥样硬化具有重要意义。     

血管内皮功能与血管重塑

血管内皮具有强大的生理功能,内皮功能障碍参与心血管疾病的发生、发展.近年的研究表明,血管重塑对心血管疾病的意义愈见明显,而内皮细胞在血管重塑过程中发挥重要作用,内皮功能障碍可影响血管重塑的程度和性质.本文就正常血管内皮功能及其在血管重塑过程中的作用以及内皮功能障碍与血管重塑的关系作一综述.     

Endothelial dysfunction and arterial hypertension

The endothelium lines all blood vessels in the human body, it is the basic structure which ensures the action of substances circulating in the blood stream on the vascular wall. It is an organ the sound state of which is essential for the physiological function of the vascular system. Its impaired function is a basic factor in the genesis and development of vascular disease. Under physiological conditions the endothelium has antiadhesive and antithrombotic properties, it produces vasoactive substances, prevents the penetration of circulating substances and formed elements across the vascular wall, and via adhesion molecules it participates in the interaction with cells in the circulation. Risk factors of cardiovascular diseases such as hypertension, hyperlipidaemia, hyperglycaemia, smoking damage the function of endothelial cells and cause the development of endothelial dysfunction. In patients with arterial hypertension endothelial dysfunction is characterized by an impaired endothelium dependent relaxation, increased adhesion and permeability of endothelial cells, structural changes of the vascular wall. When the endothelium is damaged by released cytokines an increased expression of adhesion molecules occurs, adhesion and migration of inflammatory cells across the vascular wall. Cytoadhesion molecules are released from the surface of the endothelium into the circulation where the rise of their plasma levels can serve as a marker of endothelial damage. Endothelial dysfunction in hypertonic subjects contributes in a significant way to the development and progression of chronic vascular disease--atherosclerosis. Improvement of the damaged endothelial function is therefore at present a desirable therapeutic objective in the treatment of hypertension.     

H型高血压的病因及发病机制

H型高血压在我国发病率很高。其同型半胱氨酸水平与年龄、性别、人种、营养及合并疾病等多个因素有关;发病机制涉及到血管内皮细胞功能障碍、血管平滑肌细胞增殖、血脂异常、凝血系统异常及胰岛素抵抗等多个方面。理解这些基本影响因素,将为H型高血压的防治起到重要作用。     

中性粒细胞淋巴细胞比值与OPCABG术后新发房颤相关性研究

原发性高血压是由遗传和环境等多种因素共同作用导致的疾病,有研究表明血管内皮功能障碍是原发性高血压发病机制中的重要环节。细胞外囊泡（Extracellular Vehicles, EVs）是体液环境中存在的一种包含核酸、蛋白质等成分的脂质体,具有在细胞间信息交换的功能。EVs能够影响靶细胞的表型和功能,参与多种疾病的病理生理过程。有研究显示EVs可能在血压调节中发挥重要作用,介导血管内皮功能的变化。EVs参与细胞免疫及体液免疫造成的血管内皮损伤过程,刺激血管内皮分泌促炎症因子,损伤血管的舒张功能。同时EVs刺激内皮细胞中活性氧物质水平的增加,减少一氧化氮的产生及降低其生物利用度,直接影响内皮细胞依赖的血管舒张功能,引起血压升高。本文总结了EVs在原发性高血压血管内皮损伤中的作用,提示EVs参与原发性高血压的发生发展过程,为进一步深化高血压发病机制的相关研究提供参考。     

Inhibition of the renin angiotensin system: Implications for the endothelium

The endothelium is critically involved in modulating vascular tone through the release of vasodilator (mainly nitric oxide; NO) and vasoconstrictor agents. Under normal conditions the endothelium induces NO-mediated vasodilation, and opposes cell adhesion and thrombosis. Angiotensin II-induced generation of reactive oxygen species plays a key role in the pathophysiology of endothelial dysfunction by reducing NO bioavailability. Endothelial dysfunction is associated with several pathologic conditions, including hypertension and diabetes, and is characterized by altered vascular tone, inflammation, and thrombosis in the vascular wall. Inhibition of the renin-angiotensin-aldosterone system has induced beneficial effects on endothelial function in animals and humans. Angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and mineralocorticoid receptor antagonists have improved endothelial function in hypertension and diabetes, slowed the progression of atherosclerosis, and reduced the risk associated with cardiovascular disease.     

Vascular endothelium: target organ of cardiovascular pathologies

The endothelium plays an essential role in regulation of vascular tone. It has vasodilator, antiaggregating, anti-thrombotic and anti-inflammatory properties. In the case of endothelial dysfunction (induced by hypercholesterolaemia, hypertension and/or diabetes), all of these properties are reversed; it becomes thrombogenic, it secretes vasoconstrictor substances promoting platelet aggregation and penetration of white blood cells into the vessel wall. This endothelial dysfunction then allows the development of the atheromatous lesion. The therapeutic approach must be based on restoration of the normal physiological properties of the endothelium.     

Vascular Endothelial Function and Hypertension: Insights and Directions

Hypertension contributes significantly to worldwide cardiovascular morbidity and mortality. Hypertension appears to have a complex association with endothelial dysfunction, a phenotypical alteration of the vascular endothelium that precedes the development of adverse cardiovascular events and portends future cardiovascular risk. This review concentrates on recent findings with respect to the mechanisms of hypertension-associated endothelial dysfunction, the interrelationship between these two entities, and the relationship of the efficacy of antihypertensive therapies to improvements in vascular homeostasis beyond blood pressure reduction. Current evidence suggests that hypertension and endothelial dysfunction are integrally related with respect to pathophysiologic mechanisms. Future studies will need to identify the key connections between hypertension and endothelial dysfunction to allow novel interventions to be designed and promulgated.     

阻塞性睡眠呼吸暂停低通气综合征患者高血压发病机制的研究进展

众多研究表明阻塞性睡眠呼吸暂停低通气综合征 (OSAHS)是高血压发病的独立危险因素 ,然而其高血压发病机制尚未阐明 ,神经、体液、血管内皮功能障碍、睡眠结构改变和遗传等许多因素可能与之有关。     

Persistent macrovascular and microvascular dysfunction in patients with malignant hypertension

Endothelial dysfunction is characteristic of patients with essential hypertension, but only limited data are available on different aspects of endothelial function in patients with malignant-phase hypertension. We investigated myocardial perfusion using real-time quantitative myocardial contrast echocardiography with concurrent assessment of macrovascular and microvascular endothelial damage/dysfunction in patients with previous malignant hypertension (but now in stable phase), who were compared with patients with treated "high-risk" hypertension (hypertension) and healthy controls. We measured flow (hyperemia)-mediated dilation and response to glyceryl trinitrate of brachial artery (ultrasound), microvascular (forearm) response to acetylcholine and sodium nitroprusside (laser Doppler), pulse wave velocity, circulating endothelial and endothelial progenitor cells in 15 patients with malignant hypertension, 40 matched patients with hypertension, and 40 healthy controls. Patients with malignant hypertension had impaired endothelial-dependant response to acetylcholine (P<0.001, but not to sodium nitroprusside) compared with hypertension and impaired reaction to both stimuli compared with healthy subjects (P<0.001). Patients with malignant hypertension had increased circulating endothelial cells (P=0.001), endothelial progenitors (P=0.008), and stiffness (P=0.003). Both hypertensive groups had impaired response to hyperemia and glyceryl trinitrate when compared with healthy controls (P<0.05). Both hypertensive groups had similar myocardial perfusion, which was significantly lower than in healthy controls. There were no significant differences in hyperemia and endothelium-independent stimuli between the 2 hypertensive groups. In conclusion, despite fairly well-controlled blood pressure, malignant hypertension patients had more pronounced abnormalities of macrovascular and microvascular function (which seem to be both endothelium dependent and endothelium independent) compared with patients with hypertension and healthy controls.     

单纯收缩期高血压患者血清晚期糖基化终产物与血管功能的关系

目的探讨晚期糖基化终末产物(AGEs)与血流介导的内皮依赖性血管舒张功能(FMD)间的关系及其致血管功能异常的作用。方法选择单纯收缩期高血压(ISH)患者120例作为ISH组,双期高血压患者120例作为双期高血压(DH)组,年龄配对的健康人群70例作为正常对照组,采用日本科林公司生产的VP1000动脉硬化检测仪测定颈股动脉脉搏波传导速度(cfPWV),超声技术测定FMD,ELISA检测受试者外周血清中AGEs和内皮素1,Griess法测定外周血中一氧化氮含量。结果ISH组的cfPWV、AGEs、内皮素1高于DH组及正常对照组(P<0.05);ISH组及DH组FMD、一氧化氮低于正常对照组(P<0.05),而FMD、一氧化氮在ISH组及DH组间差异无统计学意义;AGEs与cfPWV、内皮素1呈正相关(r=0.525,P<0.01;r=0.863,P<0.01);AGEs与FMD、一氧化氮呈负相关(r=-0.635,P<0.01;r=-0.669,P<0.01);多元逐步回归分析显示AGEs、cfPWV是FMD的危险因素。结论AGEs是导致血管功能异常的危险因素,可能在ISH的发生发展过程中起一定作用。     

Endothelial dysfunction in arterial hypertension

Systemic arterial pressure is a dynamic and reactive physiological parameter depending on a great many factors. The endothelial cells of the vascular system are responsible for many biochemical reactions maintaining vascular homeostasis and therefore arterial pressure. Arterial hypertension, atherosclerosis and endothelial dysfunction constitute risk factors increasing morbidity and mortality of cardiovascular origin. These three elements are closely related and frequently act simultaneously damaging different organs. In this paper we review the physiology of the endothelium and the probable consequences of endothelial dysfunction on the pathophysiology of arterial pressure.