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Blood vessels and the endothelium 

Blood vessels and the endothelium

Blood vessels and the endothelium

Patrick Vallance

and Keith Channon



Nitric oxide synthase uncoupling and endothelial dysfunction. Perivascular adipose tissue adipocytokine release in vascular pathophysiology.

Updated on 29 Oct 2015. The previous version of this content can be found here.
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date: 28 April 2017

Anatomy of blood vessels

The blood vessel wall consists of the intima, the media, and the adventitia. Not all vessels have each layer, and the layers vary in size and structure between vessels. (1) The intima is made up of a single layer of endothelial cells on a basement membrane, beneath which—depending on vessel size—there may be a layer of fibroelastic connective tissue and an internal elastic lamina that provides both structure and flexibility. Embedded in the intima are pericytes. (2) The media is made up of smooth muscle cells, elastic laminae and extracellular matrix. (3) The adventitia is the outermost part of the vessel, composed mainly of fibroelastic tissue but also containing nerves, small feeding blood vessels (the vasa vasorum), and lymph vessels. The adventitia is directly related to the surrounding perivascular adipose tissue.

Function of particular constituents of blood vessels

Endothelial cells are metabolically very active and exert a profound influence on vascular reactivity, thrombogenesis and coagulation, and the behaviour of circulating cells. They produce key vasodilator mediators: nitric oxide (NO), prostanoids, and hyperpolarizing factor. Although the predominant influence of the healthy endothelium is as dilator, it also produces important vasoconstrictor factors, including endothelin, angiotensin-converting enzyme (ACE), certain prostanoids, and reactive oxygen species (ROS) such as superoxide anion.

The endothelium synthesizes and releases prothrombotic and antithrombotic factors, with antithrombotic factors predominating under basal conditions. It also prevents cells from adhering fully to the vessel wall, but allows leucocytes to roll along its surface.

Vascular smooth muscle cells—are remarkably plastic and may adopt a range of phenotypes: they can leave the quiescent, contractile state and enter a replicative state, undergo cell death through apoptosis, migrate into the intima, adopt a secretory phenotype that results in matrix deposition (including developing bone-like features and calcification), and can contribute to inflammation within the vessel wall.

The vessel is surrounded by adventitia and perivascular adipose tissue (PVAT), which contain adipocytes, inflammatory cells, and fibroblasts. Evidence suggests that there is continuous cross-talk between the vascular wall and perivascular tissues. PVAT secretes a wide range of adipocytokines, that have paracrine effects on the vessel wall. The vessel and its PVAT are now considered to be closely interrelated, with PVAT playing important roles in vascular homeostasis and pathophysiology.

Integrated responses of blood vessels

Blood flow elicits an endothelium-dependent dilator tone due to the production of NO, which provides a physiological counterbalance to the constrictor tone of the sympathetic nervous system. Veins differ from arteries and arterioles, and do not seem to be actively dilated by continuous release of NO.

Flow-mediated dilatation is an autoregulatory property of blood vessels that tends to oppose classical myogenic autoregulation—the process by which a blood vessel constricts in response to an increase in intraluminal pressure. There is a fourth-power relationship between resistance to flow and the radius of a blood vessel, which means that relatively small changes in the thickness or contractile state of smooth muscle in small arteries and arterioles have big effects on systemic vascular resistance.

There are important interactions between the sympathetic nervous, renin–angiotensin, and endothelin systems, with these acting in concert to control constrictor tone, and with the endothelin system providing a slowly modulating, background constrictor tone. Additional endocrine signals that modulate vascular tone and function include circulating cortisol and oestrogens.


Several clinical conditions—including atherosclerosis, hypertension, hypercholesterolaemia, and diabetes—are associated with reduced NO-mediated effects. Overproduction of NO may also contribute to disease, with induction of inducible NO synthase, e.g. in sepsis leading to production of large amounts of NO and resulting in vascular paresis. Expression of adhesion molecules by the vascular endothelium is an important mechanism of cellular adhesion during inflammation and is also important in recruitment of T cells and monocytes in atherosclerosis. Impaired production and/or function of endothelial progenitor cells, particularly with ageing, may contribute to the pathogenesis of endothelial dysfunction in disease, particularly in atherosclerosis.

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