title: [Endothelial dysfunction and arterial hypertension].
abstract: The endothelium lines all blood vessels in the human body, it is the basic structure which ensures the action of substances circulating in the blood stream on the vascular wall. It is an organ the sound state of which is essential for the physiological function of the vascular system. Its impaired function is a basic factor in the genesis and development of vascular disease. Under physiological conditions the endothelium has antiadhesive and antithrombotic properties, it produces vasoactive substances, prevents the penetration of circulating substances and formed elements across the vascular wall, and via adhesion molecules it participates in the interaction with cells in the circulation. Risk factors of cardiovascular diseases such as hypertension, hyperlipidaemia, hyperglycaemia, smoking damage the function of endothelial cells and cause the development of endothelial dysfunction. In patients with arterial hypertension endothelial dysfunction is characterized by an impaired endothelium dependent relaxation, increased adhesion and permeability of endothelial cells, structural changes of the vascular wall. When the endothelium is damaged by released cytokines an increased expression of adhesion molecules occurs, adhesion and migration of inflammatory cells across the vascular wall. Cytoadhesion molecules are released from the surface of the endothelium into the circulation where the rise of their plasma levels can serve as a marker of endothelial damage. Endothelial dysfunction in hypertonic subjects contributes in a significant way to the development and progression of chronic vascular disease--atherosclerosis. Improvement of the damaged endothelial function is therefore at present a desirable therapeutic objective in the treatment of hypertension.
authors.affiliation: II. interní klinika 1. LF UK a VFN, Praha.
authors.forename: Z
authors.initials: Z
authors.lastname: Marecková
authors.forename: S
authors.initials: S
authors.lastname: Heller
authors.forename: K
authors.initials: K
authors.lastname: Horký
mesh_terms: D001161:Arteriosclerosis / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*