Abstract
Hypertension (HTN) is one of the most prevalent diseases worldwide and is among the most important risk factors for cardiovascular and cerebrovascular complications. It is currently thought to be the result of disturbances in a number of neural, renal, hormonal, and vascular mechanisms regulating blood pressure (BP), so crucial importance is given to the imbalance of a number of vasoactive factors produced by the endothelium. Decreased nitric oxide production and increased production of endothelin-1 (ET-1) in the vascular wall may promote oxidative stress and low-grade inflammation, with the development of endothelial dysfunction (ED) and increased vasoconstrictor activity. Increased ET-1 production can contribute to arterial aging and the development of atherosclerotic changes, which are associated with increased arterial stiffness and manifestation of isolated systolic HTN. In addition, ET-1 is involved in the complex regulation of BP through synergistic interactions with angiotensin II, regulates the production of catecholamines and sympathetic activity, affects renal hemodynamics and water–salt balance, and regulates baroreceptor activity and myocardial contractility. This review focuses on the relationship between ET-1 and HTN and in particular on the key role of ET-1 in the pathogenesis of ED, arterial structural changes, and impaired vascular regulation of BP. The information presented includes basic concepts on the role of ET-1 in the pathogenesis of HTN without going into detailed analyses, which allows it to be used by a wide range of specialists. Also, the main pathological processes and mechanisms are richly illustrated for better understanding.
Highlights
Hypertension (HTN) is one of the most prevalent socially significant diseases and is among the most important preventable risk factors for other diseases [1]
It is currently thought to be the result of disturbances in a number of neural, renal, hormonal, and vascular mechanisms regulating blood pressure (BP) [4], as crucial importance is given to the imbalance of a number of vasoactive substances, some of which are produced from the vascular endothelium [5]
In one classic experiment in which mice overexpressing human pre-proET-1 in the endothelium have been crossed with atherosclerosis-prone mice and fed a high-fat diet, the lipid-containing plaques in crossed animals have been increased dramatically more than in E −/− mice, along with an increase in BP. These findings suggest that increased endothelial expression of ET-1 accelerates the progression of atherosclerosis and may be the link between atherosclerosis and HTN [120]
Summary
Hypertension (HTN) is one of the most prevalent socially significant diseases and is among the most important preventable risk factors for other diseases [1]. In 40% of adults, a genetically prohypertensive phenotype is present or is the result of partially epigenetically mediated environmental effects This is related to the predominance of vasoconstrictor actions of ET-1 mediated by ETA and ETB2 in VSMC, which is due to the hypertensive effect of increased endothelial expression of the ET-1 gene (EDN1) [19]. Low doses of ET-1 infused into the brachial artery cause vasodilatation, consistent with ETB-mediated release of vasodilators, but this was followed by sustained vasoconstriction of the forearm vascular bed at higher doses because the peptide accessed the smooth muscle ETA receptors [20]. In patients with essential HTN, the activity of exogenous ET-1 is increased, similar, or decreased compared to normotensive subjects, depending on which vascular district or scheme of administration is considered [21]
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