Endothelial dysfunction over the course of coronary artery disease - PubMed (original) (raw)

Endothelium-derived vasoactive substances. Shear stress and activation of a variety of receptors leads to a release of nitric oxide by inducing endothelial nitric oxide synthase. It exerts relaxation of vascular smooth muscle cells and exerts antiproliferative effects as well as inhibits thrombocyte aggregation and leucocyte adhesion. Other endothelium-derived relaxing factors, including endothelium-derived hyperpolarizing factor and prostacyclin, are also shown. ACE, angiotensin-converting enzyme; Ach, acetylcholine; AI, angiotensin I; AII, angiotensin II; AT1, angiotensin 1 receptor; Bk, bradykinin; COX, cyclooxygenase; ECE, ET-converting enzyme; EDHF, endothelium-derived hyperpolarizing factor; ETA and ETB, endothelin A and B receptors; ET-1, endothelin-1;

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-arginine; M, muscarinic acetylcholine receptor; PGH2, prostaglandin H2; ROS, reactive oxygen species; S1, serotoninergic receptor; TX, thromboxane receptor; TXA2, thromboxane; 5-HT, serotonin. Reproduced with kind permission from Springer Science and Business Media. Source: Springer. Pflügers Arch- Eur J Physiol (2010) 459:1005–1013. Human endothelial dysfunction: EDRFs. Flammer and Lüscher.