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Endothelial dysfunction: the first step toward coronary arteriosclerosis Vanhoutte PMCirc J 2009[Apr]; 73 (4): 595-601The endothelium causes relaxations of the underlying vascular smooth muscle, by releasing nitric oxide (NO). The endothelial cells also can evoke hyperpolarization of the vascular smooth muscle cells (endothelium-dependent hyperpolarizations, endothelium-derived hyperpolarizing factors-mediated responses). Endothelium-dependent relaxations involve both pertussis toxin-sensitive Gi and pertussis toxin-insensitive Gq coupling proteins. The endothelial release of NO is reduced in diabetes and hypertension. Arteries covered with regenerated endothelium lose the pertussis-toxin sensitive pathway for NO-release. This dysfunction favors vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis. Endothelial cells also release endothelium-derived contracting factors (EDCF). Most endothelium-dependent contractions are mediated by vasoconstrictor prostanoids (endoperoxides and prostacyclin), which activate thromboxane-prostanoid (TP)-receptors of the underlying vascular smooth muscle cells. EDCF-mediated responses are augmented by aging, hypertension and diabetes. Thus, endothelial dysfunction is the first step toward coronary arteriosclerosis.|Animals[MESH]|Cell Polarity[MESH]|Coronary Artery Disease/*etiology/*metabolism/physiopathology[MESH]|Coronary Vasospasm/metabolism/physiopathology[MESH]|Diabetes Mellitus/metabolism/physiopathology[MESH]|Endothelial Cells/metabolism[MESH]|Endothelium, Vascular/*metabolism/physiopathology[MESH]|GTP-Binding Protein alpha Subunits, Gi-Go/metabolism[MESH]|GTP-Binding Protein alpha Subunits, Gq-G11/metabolism[MESH]|Humans[MESH]|Hypertension/metabolism/physiopathology[MESH]|Macrophages/metabolism[MESH]|Muscle Relaxation[MESH]|Muscle, Smooth, Vascular/*metabolism/pathology/physiopathology[MESH]|Nitric Oxide/metabolism[MESH]|Thrombosis/metabolism/physiopathology[MESH]|Vasoconstrictor Agents/metabolism[MESH] |
