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。     

阻塞性睡眠呼吸暂停综合征与血管内皮功能障碍研究进展

阻塞性睡眠呼吸暂停综合征(obstructive sleep apnea hypopnea syndrome,OSAHS)是高血压、动脉粥样硬化等心血管疾病发病的重要危险因素之一,虽然目前机制尚未完全阐明,但与内皮功能障碍密切相关.本文就正常血管内皮功能、内皮功能障碍及评价方法 发、OSAHS与内皮功能障碍及治疗等进行综述.     

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。     

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.     

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。     

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。     

叶酸干预血管内皮功能障碍的研究进展

血管内皮功能障碍与诸多心血管疾病的发生、发展有密切联系,被认为是心血管疾病危险的终点替代指标。内皮功能障碍的研究和血管内皮的保护成为目前研究的热点。叶酸,一种经济无毒的药物,能明确改善血管内皮功能。其可能机制有降低血浆同型半胱氨酸、抗氧化作用、对内皮型一氧化氮合酶作用等,其对心血管疾病的预防具有重要意义。     

血管内皮细胞功能紊乱与血管老化

血管老化指血管结构和功能的退行性改变,引起动脉硬化,导致循环障碍,是冠心病、心绞痛、心肌梗死、高血压等心血管疾病的病理基础.血管老化的研究目前主要集中在血管内皮细胞以及活性物质改变.本文综述了血管内皮功能障碍以及与动脉粥样硬化等内容.     

高游离脂肪酸血症对不同糖耐量水平老年人血管内皮功能的影响

血管内皮功能障碍是动脉粥样硬化（AS）的早期改变,与高血压、糖耐量受损或糖尿病、肥胖、脂代谢紊乱和吸烟等有关[1].血管内皮功能的评价已成为AS诊断的重要依据之一.高游离脂肪酸（FFAs）血症是代谢综合征患者的一个普遍现象,我们通过测定不同血糖和不同糖耐量水平老年人FFAs水平以及应用高分辨血管外彩色多普勒仪进行肱动脉内皮依赖性血管舒张功能的评价,旨在分析FFAs与内皮功能之间的关系及临床意义。     

老年原发性高血压患者肱动脉血流介导的内皮依赖性舒张功能的变化

<正>高血压患者的临床表现常以动脉舒张压或(和)收缩压增高,并伴有心、脑、肾及视网膜等器官功能性改变〔1〕。高血压的发病机制十分复杂至今尚未完全阐明,而越来越多的研究证实,血管内皮功能障碍与高血压的发生和发展存在十分密切的关系。老年原发性高血压患者存在内皮功能损伤,肱动脉血流介导的血管舒张功能障碍(FMD)是高血压形成的主要机制和发病环节之一〔2〕。但有关原发性高血压1、2、3级患者肱动     

Different effects of antihypertensive drugs on endothelial dysfunction

Since endothelial dysfunction may significantly contribute to the pathophysiology of hypertension and its complications, its modification seems to be a very attractive means to favourably affect the development of atherosclerosis and cardiovascular events in hypertensive patients. However, not all antihypertensive drugs consistently improve endothelial dysfunction. While first-generation beta-blockers showed contrasting or null effects on endothelial function, newer beta-blockers of the third generation, such as carvedilol and nebivolol, seem to be provided with specific endothelium-mediated vasodilating effects. Calcium channel blockers are generally able to increase endothelium-dependent vasodilation in several vascular beds, in patients with essential hypertension, probably through multiple mechanisms. Most studies have shown thatACE inhibitors favourably affect endothelial function mainly in the subcutaneous, epicardial and renal circulation, not only by inhibiting the effects of angiotensin II on the endothelium, but also by enhancing bradykinin-induced vasodilation, probably a hyperpolarization-related effect. On the other hand, discordant evidence is available about the effects of angiotensin II receptor type I blockers on endothelial function in patients with essential hypertension, atherosclerosis or diabetes.There are data suggesting that an increased activity of the endothelin- I system may play a role in the blunted endothelium-dependent vasorelaxation of hypertensive patients, an effect that could be contrasted by the use of endothelin-I receptor antagonists. However, to date no substantial clinical efficacy of endothelin-I receptor blockers has been shown in patients with essential hypertension. Finally, other possibly useful compounds in restoring impaired endothelial function in hypertension are some antioxidant agents such as vitamin C, folic acid, the cofactor tetrahydrobiopterin (BH4), L-arginine and the drugs of the statin class.     

Vascular endothelial dysfunction in cirrhosis

Endothelial dysfunction is regarded as an early key event in multiple diseases. The assessment of vascular nitric oxide (NO) level is an indicative of endothelial dysfunction. In liver cirrhosis, on one hand, endothelial dysfunction is known as impaired endothelium-dependent relaxation in the liver microcirculation and contributes to increased intra-hepatic vascular resistance, leading to portal hypertension. On the other, increased production of vasodilator molecules mainly NO contributes to increased endothelium-dependent relaxation in the arteries of the systemic and splanchnic circulation. The aims of this review are to summarize and discuss: (1) unique characteristics of sinusoidal endothelial cell (SECs) and SEC dysfunctions in cirrhosis, and (2) endothelial dysfunctions in the arterial splanchnic and systemic circulation in cirrhosis with portal hypertension.     

Endothelial dysfunction in normotensive Chinese with a family history of essential hypertension

Endothelial dysfunction is seen in patients with essential hypertension. However, it is still debated whether impaired endothelial function occurs before the development of hypertension. The aim of our study was to investigate whether endothelial dysfunction occurs in genetically vulnerable normotensive Chinese, and whether the endothelial dysfunction is worse as essential hypertension progresses. Endothelial function was assessed by high-resolution vascular ultrasound (7.5 MHz). The diameters of brachial arteries were measured at rest, during reactive hyperemia, and after sublingual administration of nitroglycerine (GTN) in 58 subjects with a mean age of 46.7 +/- 10.1 years. Among them, 18 patients had essential hypertension (Group 2), 20 normotensive subjects had a family history of hypertension (Group 3), and 20 normotensive subjects without a family history of cardiovascular diseases served as controls (Group 1). There was no difference in age among the three groups (Group 1: 46.5 +/- 10.5 versus Group 2: 46.7 +/- 9.5 versus Group 3: 44.50 +/- 11.21 years, P = NS). Flow-mediated dilatation of brachial arteries was significantly reduced in Group 2 and 3 as compared with Group 1 (Group 1: 13.2 +/- 5.9% versus Group 2: 8.0 +/- 3.6 versus Group 3: 4.86 +/- 3.5, both p < .01). On the other hand, nonflow mediated vasodilatation in response to GTN did not differ among the three groups. Endothelium-dependent vasodilatation is impaired not only in normotensive subjects with a family history of hypertension, but also becomes worse in the hypertensive patients.     

Endothelial dysfunction in patients with exaggerated blood pressure response during treadmill test

BACKGROUND: The diagnostic and prognostic importance of exaggerated blood pressure response to exercise is controversial. Endothelial dysfunction has been demonstrated in patients with atherosclerosis and risk factors for coronary artery disease, but there is a paucity of information on patients with exercise-induced hypertension. HYPOTHESIS: We designed the study to evaluate endothelial function in patients with exaggerated blood pressure response during exercise. METHODS: Exercise-induced hypertension was defined as systolic blood pressure > or = 210 mmHg in men and > or = 190 mmHg in women during the treadmill test. Using a high-resolution ultrasound technique, endothelial function of the brachial artery in patients with exercise-induced hypertension (n = 25) and control subjects (n = 25) was investigated. RESULTS: Endothelium-dependent vasodilation was impaired in patients with exercise-induced hypertension compared with controls (7.77 +/- 5.14 vs. 2.81 +/- 2.29%, p < 0.05). On univariate analysis, the extent of vasodilation correlated negatively with age (r = -0.43, p < 0.05) and delta systolic blood pressure (r = -0.39, p < 0.05). Even after adjustment for factors known to affect endothelial function, endothelium-dependent vasodilation was decreased in patients with exercise-induced hypertension (beta = 5.375, p = 0.02). CONCLUSION: Patients with exercise-induced hypertension have impaired endothelium-dependent vasodilation. This study also supports the concept that endothelial dysfunction may play an important role in exercise-induced hypertension.     

Kidney and Hypertension—Causes

Renal disease is closely associated with hypertension. On the one hand, kidney disease provokes hypertension. On the other hand, hypertension aggravates the progression of renal dysfunction. The pathomechanisms through which the kidney raises blood pressure have been considerably clarified in recent years. In experimental and clinical studies, it could be shown that "hypertension goes with the kidney". This suggests that some renal anomalies predispose to hypertension. Recently, it could be shown that the kidneys of individuals with so-called essential hypertension have less glomeruli than the kidneys of control individuals. In renal patients the kidney raises blood pressure through several mechanisms. First, the pressure-natriuresis relationship is shifted to the right, i. e., sodium excretion requires higher renal perfusion pressures. Second, there is inappropriate activation of the renin-angiotensin system. Third, as only recently documented in detail, renal injury raises the sympathetic tone, even when whole kidney glomerular filtration rate (GFR) is unchanged. This results from stimulating afferent signals emanating from the kidney. Fourth, there is evidence of impaired endothelial cell dependent vasodilatation even in very early stages of renal dysfunction. Fifth, the pulse pressure profile is altered as a consequence of premature and accelerated aging causing stiffening of the aorta. Knowledge of these pathomechanisms is important for selection of appropriate antihypertensive treatment.     

Renal endothelial dysfunction and hypertension

Patients with essential hypertension have an impaired endothelium-dependent vascular relaxation in the renal arteries. The possible mechanisms by which essential hypertension is associated with alterations in endothelial function are decreased endothelial nitric oxide (NO) synthase activity, decreased availability or deficiency of L-arginine, increased endogenous NO synthase inhibitor, inactivation of NO by superoxide anions, and increased vasoconstrictors. However, the precise mechanism is not known. In addition, we are now confronted with a difficult question. And the question is whether endothelial dysfunction is a cause or consequence of hypertension. We hypothesize that the initial endothelial dysfunction raises blood pressure, and the development of hypertension impairs much more endothelial function, resulting in constituting the vicious cycle between endothelial dysfunction and hypertension. However, at the moment, it is impossible to answer this question with any certainty. Impairment of endothelial function has been shown to play a critical role in the development and maintenance of hypertension. It is clinically important to select an appropriate intervention that is effective in improving endothelial dysfunction in patients with essential hypertension. Several investigators including us have demonstrated that certain interventions improve endothelial dysfunction of forearm and renal circulation in patients with essential hypertension: angiotensin-converting enzyme inhibitors; lifestyle modification: exercise, body weight reduction, and sodium reduction; estrogen replacement in postmenopausal women; and novel properties: vitamin C and tetrahydrobiopterine. In patients with essential hypertension, endothelial function is impaired in several arteries. However, endothelial dysfunction in essential hypertension is reversible. We can restore endothelial function in essential hypertensive patients.     

The role of statins in endothelial dysfunction in hypertension

PURPOSE OF REVIEW: Hypertension and dyslipidemia frequently coexist, and endothelial dysfunction is associated with the pathophysiology of both atherosclerosis and hypertension. Evidence is convincing for an overlapping role of oxidative stress, renin-angiotensin system activation, and dyslipidemia in the genesis of endothelial dysfunction. RECENT FINDINGS: Ample experimental and human data suggest that common cellular pathways are involved in the pathogenesis of hypertension, increased vascular resistance, and plaque formation. Multiple interventions such as dietary modification, exercise, antioxidants, and antihypertensive drugs improve endothelial dysfunction in hypertension. Statin drugs are a cornerstone of dyslipidemia therapy. Studies have demonstrated that statins correct endothelial function and vascular stiffening and may be useful in reducing blood pressure to target levels. SUMMARY: Statins may be a useful adjunct in the treatment of hypertension in patients with dyslipidemia and possibly those with normal cholesterol levels.     

原发性高血压血管内皮细胞损害机制的研究和治疗进展

血管内皮是人体最大的内分泌、旁分泌器官,有重要生理功能,内皮功能不全与高血压密切相关。现综述高血压与内皮功能紊乱之间相互作用的病理生理机制以及在高血压治疗中改善内皮功能的思路。     

原发性高血压与内皮功能研究进展

高血压可以导致并加重内皮功能紊乱,而内皮功能紊乱又促进高血压的发生和发展。现综述高血压与内皮功能紊乱之间相互作用的病理生理机制、内皮功能的检测方法以及在高血压治疗中改善内皮功能的思路。     

Role of MicroRNA in Endothelial Dysfunction and Hypertension

Purpose of Review

Hypertension is either a cause or a consequence of the endothelial dysfunction and a major risk factor for cardiovascular disease (CVD). In vitro and in vivo studies established that microRNAs (miRNAs) are decisive for endothelial cell gene expression and function in various pathological conditions associated with CVD.This review provides an overview of the miRNA role in controlling the key connections between endothelial dysfunction and hypertension.

Recent Findings

Herein we summarize the present understanding of mechanisms underlying hypertension and its associated endothelial dysfunction as well as the miRNA role in endothelial cells with accent on the modulation of renin-angiotensin-aldosterone-system, nitric oxide, oxidative stress and on the control of vascular inflammation and angiogenesis in relation to endothelial dysfunction in hypertension. In particular, latest insights in the identification of endothelial-specific microRNAs and their targets are added to the understanding of miRNA significance in hypertension.

Summary

This comprehensive knowledge of the role of miRNAs in endothelial dysfunction and hypertension and of molecular mechanisms proposed for miRNA actions may offer novel diagnostic biomarkers and therapeutic targets for controlling hypertension-associated endothelial dysfunction and other cardiovascular complications.