[The role of endothelium in hypertension and atherosclerosis]

Endothelium was "discovered" as a separate organ in the last decades of the previous century. For a long time endothelial cells were considered as a very passive monolayer of cells just covering the inner part of vascular walls. The role of these cells was thought to be only a mechanical barrier between circulating blood and vascular structures. Nowadays, after a series of biochemical and experimental studies, one can name endothelium as an organ, covering approximately 700 sqaure meters, weighing about 1.5 kilos in an average male with weight of 70 kg. Not only its quantity, but also its function is amazing. The most prominent and first well studied function of endothelial cells is vasodilatation and vasoconstriction. Normal cells, which are intact and in function produce regularly one of the most important protecting agent in circulation: NO. Normal endothelial cells produce NO as a result of higher blood pressure or growing demand for oxygen. It is produced from aminoacid L-arginine as a result of enzyme activity: endothelial NO synthetase (eNOS). Interleukins also can increase production of NO. NO has also antiinflammatory efects, helping in reparation and healing processes. Prostacyclins are the second most important vasodilating agent produced in endothelium. On the other hand, vasoconstriction is also mediated via endothelium. Endothelin 1, angiotensin II and thromboxan A are produced in vascular wall by endothelial cells, acting as opponent to NO. ACE system is very active inside those cells, with permanent local angiotensin II formation, that mostly act on vascular wall itself. Effects of such generated angiotensin II stimulate activation of VCAM molecules, starting adhesion of monocytes, their penetration in vascular wall and activation. Acivated macrophages get in contact with oxidized LDL particles already inside the vascular wall, producing foam cells. That is the very begining of atherosclerosis. All negative effects of excess of angiotensin II should be reduced by effective therapy with ACE inhibitors or AT antagonists. Today it seems more important to act on excess in endothelial AII in order to regulate not only blood pressure, but long-term devastating effects on target organs, preventing atherosclerosis.