Anatomy of blood vessels
There are three basic layers to blood vessels—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 comprises a single layer of endothelial cells on a basement membrane, beneath which—depending on vessel size—there may be a layer of fibro-elastic 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 predominantly of smooth muscle cells, but also has elastic fibres and...
Anatomy of blood vessels
There are three basic layers to blood vessels—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 comprises a single layer of endothelial cells on a basement membrane, beneath which—depending on vessel size—there may be a layer of fibro-elastic 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 predominantly of smooth muscle cells, but also has elastic fibres and contains the external elastic lamina. (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.
Function of particular constituents of blood vessels
Endothelial cells are metabolically very active and exert a profound influence on vascular reactivity, thrombogenesis and coagulation the behaviour of circulating cells. They produce at least three key vasodilator mediators: nitric oxide, prostanoids, and hyperpolarizing factor. Although the predominant background influence of the endothelium is as dilator, it also produces important vasoconstrictor factors, including endothelin, angiotensin-converting enzyme, certain prostanoids, and the 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—these are remarkably plastic and may adopt a range of phenotypes: they can leave the quiescent, contractile state and enter a replicative state, migrate into the intima, adopt a secretory phenotype that results in matrix deposition (including developing bone-like features and calcification), and under some conditions, can contribute to inflammation within the vessel wall.
Vascular resistance—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.
Integrated responses of blood vessels
Basal endothelium-dependent dilator tone is due to the production of nitric oxide and seems to provide a physiological counterbalance to the continuous 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 nitric oxide.
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 are important interactions between the sympathetic nervous, the renin–angiotensin, and the 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 a functional loss of nitric oxide-mediated effects. Overproduction of nitric oxide may also contribute to disease, with induction of inducible nitric oxide synthase by sepsis leading to production of large amounts of nitric oxide 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 (EPCs), particularly with aging, may contribute to the pathogenesis of endothelial dysfunction in disease, particularly in atherosclerosis.
Chapter. 9283 words. Illustrated.
Subjects: Cardiovascular Medicine
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