Abstract :
The cardiovascular system is regulated by neuronal influences, circulating hormones as well as paracrine and autocrine mechanisms in the blood vessel wall. Endothelial factors play a primary role by releasing substances which can regulate vascular tone and structure as well as adhesion of circulating blood cells. Prostacyclin (PGI2) activates cAMP and is a vasodilator and platelet inhibitor function. Nitric oxide (NO) formed from L-arginine via the activity of endothelial NO synthase (eNOS). Platelets also express eNOS. eNOS is increased in its expression by shear stress and estrogen and possibly other factors. The L-arginine nitric oxide pathway also is stimulated by shear stress as well as receptor-operated mechanisms (i.e. acetylcholine, histamine, bradykinin, substance P, ATP/ADP and thrombin). NO acts as a vasodilator and platelet inhibitor via cGMP. Furthermore, endothelial cells produce constricting factors such as endothelin-1 (ET1), thromboxane A2 and prostaglandin H2. ET1 activates ETA- and ETB-receptors on vascular smooth muscle to cause contraction and endothelial ETB-receptors cause vasodilation (by NO and PGI2). In vascular smooth muscle cells, NO is an inhibitor and ET1 a stimulator of migration and proliferation.
The endothelium is a target and mediator of cardiovascular disease and may exhibit profound dysfunction as cardiovascular disease progresses.
