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Calcification forms among vascular smooth muscle cells of the surrounding muscular layer, specifically in the muscle cells adjacent to atheromas and on the surface of atheroma plaques and tissue. [70] In time, as cells die, this leads to extracellular calcium deposits between the muscular wall and outer portion of the atheromatous plaques.
The main endogenous agonist of these cell receptors is norepinephrine (NE). The adrenergic receptors exert opposite physiologic effects in the vascular smooth muscle under activation: alpha-1 receptors. Under NE binding alpha-1 receptors cause vasoconstriction (contraction of the vascular smooth muscle cells decreasing the diameter of the ...
Lesions reflect leakage of plasma components across vascular endothelium and excessive extracellular matrix production by smooth muscle cells, usually secondary to hypertension. [ 11 ] Hyaline arteriolosclerosis is a major morphologic characteristic of benign nephrosclerosis , in which the arteriolar narrowing causes diffuse impairment of renal ...
Moreover, NO is involved in paracrine signalling between the endothelium and the smooth muscle that maintains vascular tone; without it, the muscle will not relax, and the blood vessel remains constricted. Thus, oxidized LDL also contributes to the hypertension often seen with atherosclerosis.
Nitric oxide (NO) suppresses platelet aggregation, inflammation, oxidative stress, vascular smooth muscle cell migration and proliferation, and leukocyte adhesion. [6] A feature of endothelial dysfunction is the inability of arteries and arterioles to dilate fully in response to an appropriate stimulus, such as exogenous nitroglycerine , [ 5 ...
Macrophages within the atherosclerotic legion area have a decreased ability to migrate, which further promotes plaque formation as they are able to secrete cytokines, chemokines, reactive oxygen species (ROS) and growth factors that stimulate modified lipoprotein uptake and vascular smooth muscle cell (VSMC) proliferation.
Mural cells are the vascular smooth muscle cells (vSMCs), and pericytes, of the microcirculation. Both types are in close contact with the endothelial cells lining the capillaries , and are important for vascular development and stability.
George Nikov Chaldakov (Bulgarian: Георги Ников Чалдъков) born February 23, 1940, in Burgas, Bulgaria, is a Bulgarian vascular biologist well known for his contributions to the study of secretory function of vascular smooth muscle cells, and the role of neurotrophins and perivascular adipose tissue in pathogenesis of atherosclerosis. [1]
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