Untitled

Abstract

The endothelium is a thin monocelular layer that covers all the inner surface of the blood vessels, separating the circulating blood from the tissues. It is not an inactive organ, quite the opposite. It works as a receptor-efector organ and responds to each physical or chemical stimulus with the release of the correct substance with which it may maintain vasomotor balance and vascular-tissue homeostasis. It has the property of producing, independently, both agonistic and antagonistic substances that help to keep homeostasis and its function is not only autocrine, but also paracrine and endocrine. In this way it modulates the vascular smooth muscle cells producing relaxation or contraction, and therefore vasodilatation or vasoconstriction. The endothelium regulating homeostasis by controlling the production of prothrombotic and antithrombotic components, and fibrynolitics and antifibrynolitics. Also intervenes in cell proliferation and migration, in leukocyte adhesion and activation and in immunological and inflammatory processes. Cardiovascular risk factors cause oxidative stress that alters the endothelial cells capacity and leads to the so called endothelial "dysfunction" reducing its capacity to maintain homeostasis and leads to the development of pathological inflammatory processes and vascular disease.There are different techniques to evaluate the endothelium functional capacity, that depend on the amount of NO produced and the vasodilatation effect. The percentage of vasodilatation with respect to the basal value represents the endothelial functional capacity. Taking into account that shear stress is one of the most important stimulants for the synthesis and release of NO, the non-invasive technique most often used is the transient flow-modulate "endothelium-dependent" post-ischemic vasodilatation, performed on conductance arteries such as the brachial, radial or femoral arteries. This vasodilatation is compared with the vasodilatation produced by drugs that are NO donors, such as nitroglycerine, called "endothelium independent". The vasodilatation is quantified by measuring the arterial diameter with high resolution ultrasonography. LaserDoppler techniques are now starting to be used that also consider tissue perfusion.There is so much proof about endothelial dysfunction that it is reasonable to believe that there is diagnostic and prognostic value in its evaluation for the late outcome. There is no doubt that endothelial dysfunction contributes to the initiation and progression of atherosclerotic disease and could be considered an independent vascular risk factor. Although prolonged randomized clinical trials are needed for unequivocal evidence, the data already obtained allows the methods of evaluation of endothelial dysfunction to be considered useful in clinical practice and have overcome the experimental step, being non-invasive increases its value making it use full for follow-up of the progression of the disease and the effects of different treatments.

Age-related ocular vascular changes

“…The endothelium is a monocellular layer covering the inner surface of the blood vessels which responds to physical and chemical stimuli. This activates the release of substances in order to maintain the vasomotor balance of the blood vessels [43]. Endothelial cells play an important role in modulating vascular tone, vascular caliber, release of nitric oxide (NO), regulation of inflammation, platelet activation and thrombosis.…”

Skin microvascular reactivity in trained adolescents

“…Endothelial dysfunction is an early event in detrimental sclerotic vascular pathophysiology (Ross 1993), and is common to cardiovascular, peripheral vascular and metabolic diseases (Meyer et al 2008;Morales et al 2005;Zhang et al 2000) prior to clinically detectable evidence of vascular disease (Mano et al 1996). A consequence of endothelial dysfunction is the diminished bioavailability of the potent vasodilator nitric oxide (NO) (Esper et al 2006), and this is associated with depressed endothelium-dependent vasodilation of the vessels (Celermajer et al 1994). The early identification of endothelial dysfunction and timely remedial intervention thereafter of improving NO-dilator function may offer anti-atherogenic benefits and may be a useful approach in the primary and secondary prevention of vascular disease later in life.…”

Dietary nitrite supplementation protects against myocardial ischemia-reperfusion injury

“…he loss of nitric oxide (NO) generation as a result of a dysfunctional vascular endothelium is an often cited correlate of heart disease (1). Continuous generation of NO is essential for the integrity of the cardiovascular system, and a decreased production and/or bioavailability of NO is central to the development of cardiovascular disorders (2,3).…”