The vascular endothelium

===Lecture Details===
Marianne Tare; Week 11 MED1022; Physiology
===Lecture Content===
Endothelium is squamous epithelial cells, lines blood vessels, heart and lymphatics, is largest endocrine organ in the body (10^13 cells), produces substances essential for body function. It has regional heterogeneity in structure and function as well as an organ specific phenotype. Intima is involved in hemostasis and thrombosis, vascular permeability, matrix synthesis, regulation of vascular tone, angiogenesis and metabolism. Media regulates vascular tone, protein synthesis and remodelling. Adventitia regulates vascularisation and innervation. Impairment causes vasoconstriction and atherothrombotic changes such as smooth muscle proliferation, expression of proinflammatory molecules, thrombosis. Endothelial dysfunction is first detectable change in vascular function in the genesis of atherosclerosis, is a risk factor for CV disease. 
Endothelial cells are arranged along the direction of blood flow. Vasodilators are NO, PGI2, EDHF. Vasoconstrictors are endothelin, thromboxane, constrictor prostaglandins, ANGII. NO is a diffusible factor, lipid soluble, has a half life of 6 seconds, synthesised by NO synthase from L-arginine. It also prevents platelet adhesion/aggregation, leukocyte adhesion. PGI2 is from COX-1, inhibits platelet aggregation. EDHF (endothelium-derived hyperpolarising factor) is used when NO and PGI are blocked, vasodilation accompanied by smooth muscle hyperpolarisation. Might dilate from diffusible factors or contact mediated, debatable. Turbulent flow causes reduced vasodilators, is pro-inflammatory and pro coagulation. ACh should cause vasodilation if healthy, if unhealthy causes vasoconstriction. Endothelium dependent vasodilation is impaired in diabetes. When coupled to BH2 it decreases NO and EDHF has limited effect. Arterioles tend to use EDHF rather than NO.
Adverse environments in utero increase CV disease in offspring and vascular dysfunction. Alcohol also affects this.
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