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Endothelial Dysfunction in Arterial Hypertension

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Endothelial Dysfunction in Arterial Hypertension Journal of Human Hypertension (2000) 14, Suppl 1, S20–S25 2000 Macmillan Publishers Ltd All rights reserved 0950-9240/00 $15.00 www.nature.com/jhh Endothelial dysfunction in arterial hypertension F Contreras, M Rivera, J Va´squez, MA De la Parte and M Velasco School of Medicine, Universidad Central de Venezuela, Venezuela Systemic arterial pressure is a dynamic and reactive and mortality of cardiovascular origin. These three physiological parameter depending on a great many fac- elements are closely related and frequently act simul- tors. The endothelial cells of the vascular system are taneously damaging different organs. In this paper we responsible for many biochemical reactions maintaining review the physiology of the endothelium and the prob- vascular homeostasis and therefore arterial pressure. able consequences of endothelial dysfunction on the Arterial hypertension, atherosclerosis and endothelial pathophysiology of arterial pressure. Journal of Human dysfunction constitute risk factors increasing morbidity Hypertension (2000) 14, Suppl 1, S20–S25. Keywords: endothelium: endothelial dysfunction; arterial hypertension; atherosclerosis; nitric oxide Introduction the vessel. In small vessels these cells possess a definite basal membrane underneath which fine The discovery of the endothelium as the main regu- elastic fibrils extend (subendothelium) establishing lator of vascular tone has produced an enormous contact with the smooth muscle cells of the media. amount of clinical research trying to explain the Such fibrils normally look like a continuous, retrac- physiology of this organ and its pathophysiology tile stripe, the inner elastic membrane. It is parti- related to arterial hypertension. cularly conspicuous in the muscle arteries of The endothelial cells of the vascular system are medium thickness disappearing into the capillaries. responsible for many biological activities that hold Collagen and elastin fibrils derive from mesenchy- vascular homeostasis. However, its dysfunction, mal cells of fibrocytic or smooth muscle type within which causes changes of modulation of the contrac- an amorphous, basal substance, rich in acid muco- tile state of a vessels smooth muscle, is according to polysacharides. The amount of collagen and basal experimental evidence closely associated with the 1,2 substance increases with age. appearance of premature arteriosclerosis and, in The media consists of smooth muscle cells and time, of arterial hypertension. The occurrence of elastic fibrils and the adventitia, the external coat of hypertension and atherosclerosis increases with 3 the arteries, is made of collagen fibrils, fibroblasts, age and in most cases arterial hypertension aggra- nervous fibrils and small blood vessels.4 The endo- vates atherosclerotic injuries present in blood ves- thelium is arranged in such a way that it forms a sels as well as accelerating pathological changes of monolayer covering the internal surface of arteries, structure and function in ‘target’ organs. Much evi- veins, lymphatic vessels, cavities and cardiac valves dence also demonstrate clearly that endothelial dys- as well as the cavernous body (corpus cavernosum) function brings about a thickening of the subendo- of the penis and clitoris, anterior eye chamber, ple- thelial sheet, increased amounts of proteins, lipids ura, lungs, and pericardial cavity, etc. Embryologi- and proinflammatory cells together with changes of cally the endothelium stems from mesoderm and viscoelastic properties of the arterial wall inducing weighs about 2 kg. The functional unit of the endo- alterations of the reactions to vasoactive stimuli. In thelium, the endothelial cell, is polyhedral in shape this review we analyse the underlying pathophysiol- showing a central thickness around 3 to 4 ␮m and ogical mechanisms that relate endothelial dysfunc- 0.1 ␮m at the edges. Usually the endothelium is tion with arterial hypertension. accompanied by a satellite cell, the periocyte, a cell present in blood and lymphatic vessels supporting What is the endothelium? and retaining the vascular tone. Usually three sheets are distinguished on the wall of any blood vessel: intima, media and adventitia. Functions of the vascular endothelium Blood vessels, except sinusoids, are covered with a The endothelium is the basic structure of the intima unique, continuous sheet of very specialized, meta- pursuing a control function on circulation through bolically active, polyhedral cells, the endothelial the production of various vasoactive substances. In cells, positioned parallel to the longitudinal axis of addition, it manufactures substances with enzy- matic and immunological activity. Likewise the Correspondence: Professor M Velasco, Torre Domus, Avenida endothelium is visualized as a highly selective per- Abraham, Lincoln c/Olimpo, Piso 6 Ofic 6A, Sabana Grande, meable barrier exerting a fundamental role upon the Caracas, Venezuela control of biochemical processes in blood, helping Endothelial dysfunction in arterial hypertension F Contreras et al S21 by this means to maintain vascular homeostasis Table 2 From endothelium released substances (Table 1). The endothelium possesses very specific charac- Vasodilators Vasoconstrictors teristics like the production of autacoids with antag- ¼ onistic effects involved in tone control and vascular Nitric oxide Angiotensin I and II ¼ Bradykinin Endothelin homeostasis. It also has regulatory influences on ¼ Prostacyclin Thromboxane A2 vascular rearrangement, fibrinolysis, adhesion of ¼ Hyperpolarizing factor Arachidonic Acid leucocytes and activated platelets to the endo- derived from endothelium Prostaglandin H2 5 ¼ Serotonin Thrombin thelium and on inflammatory processes. In ¼ response to a variety of chemical and physical stim- Histamine, Substance P Nicotine uli the endothelium produces a great deal of vasoac- Inhibitors of smooth muscle Promotors of smooth muscle tive and growth modulating substances as well as growth growth ¼ Nitric oxide Platelet-derived growth factor other factors mediating such functions as nitric ¼ Prostacyclin Basic fibroblast growth factor oxide (NO), a known vasodilator6 (Table 2). Due to ¼ Bradykinin its strategic location between circulating blood and ¼ Heparin sulfate the vessel wall the endothelium interacts with Thrombolytic factors Adhesion molecules neurohumoral cells and mediators, regulating in this ¼ Tissue-type plasminogen Leucocytes adhesion molecule way vascular contractility and cell composition. activator Intercellular adhesion molecule ¼ Stress and pulsating narrowing of the blood vessel Inhibitor I of the Blood cells adhesion molecules plasminogen activator walls are the most important stimuli for release of ¼ Thrombomodulin NO together with the release of systemic and local vasoactive substances.7 The main vasodilators released from endothelial cells include NO, bradykinin and prostacyclin. NO thelium and platelets aggregation. The endothelium is the most powerful endogenous vasodilator and it mediates the ability of the blood vessels to vary its seems to be responsible for the maintenance of basal architecture in response to haemodynamic changes. vascular tone.5,6,8 It is synthesized in the endo- Numerous works demonstrate that NO produced by thelium cells from L-arginine through the action of the endothelium is the main contributor to this NO synthetase.9 Additional properties of NO remodelling participating critically as a negative include inhibitory effects on migration of smooth regulator for the proliferation of vessels smooth muscle cells, adhesion of leucocytes to the endo- muscle in response to stimuli.10 Bradykinin is a potent vasodilator at the same time stimulating the release of NO and hyperpolariz- Table 1 Functions of the vascular endothelium ing factor derived from endothelium, both of which are vasodilatory substances.5 Bradykinin exerts its (1) Highly selective permeable barrier Regulation of plasma fluid, ions and macromolecules from and vasodilatory activity mainly through the release of to the vascular space. NO. Other effects of bradykinin are to promote the (2) Immunological, enzymatic and inflammatory function production of tissue-type plasminogen activator (t- Production of interleukine-I, which induces generation of T PA) supporting by this means the maintenance of cells. the fibrocytic balance. It also exhibits an antiaggreg- Antigen supplies to immunocompetent cells. ant effect upon the platelets through the release of Local production of angiotensin-converting enzyme (ACE). NO and prostacyclin. Promotion of production of adhesion molecules that participate in the inflammatory reaction. Apparently the inhibitors of the angiotensin-con- verting enzyme (ACE) act by accumulation of brady- (3) Detection of biochemical changes in blood and 11 maintenance of homeostasis kinin. The most important form of endothelium- Recognition of variations of pH and oxygen and CO2 derived vasoconstrictor substances comprise angio- concentration participating in this way in cardiovascular tensin II and endothelin. Angiotensin II is a power- homeostasis. ful vasoconstrictor with various effects on blood (4) Autocrine function vessel structure and on vascular homeostasis Release of vasoactive substances, which regulate vascular tone: (Figure 1).12 Nitric oxide, prostacyclin Angiotensin II increases the production of type 1 Endothelin, thromboxane Angiotensin-I and angiotensin-II inhibitor of the plasminogen activator and the pri- mary endogenous inhibitor of t-PA and promotes (5) Control of growth and cell proliferation
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