Angiotensin II HUMAN,4474-91-3,IC-0198446

Angiotensin II is a vasoconstrictor and the main bioactive peptide of the renin/Angiotensin system. Angiotensin II human plays a central role in the regulation of human blood pressure, mainly through Angiotensin II and G protein-coupled receptors(GPCRs) Angiotensin II type 1 receptor (AT1R) and Angiotensin II type 2 receptor (AT2R) interact to mediate[1].

Human induces capillary formation in endothelial cells through a LOX-1-dependent redox-sensitive pathway. Angiotensin II (1 nM) induces the expression of LOX-1 and VEGF and enhances capillary formation from human coronary endothelial cells in Matrigel assay[3,4].Angiotensin II helps to regulate overall renal tubular reabsorption of salt and water, Angiotensin II directly stimulates epithelial sodium channel activity through an AT1 receptor-dependent mechanism[8].Angiotensin II Human induces the growth of vascular smooth muscle cells, increases the synthesis of collagen type I and III in fibroblasts, leads to the thickening of the vascular wall and myocardium, and induces fibrosis. Angiotensin II also induces apoptosis[2].The effects of Angiotensin II to increase blood pressure are mediated by AT1 receptors[1], and these receptors are expressed in a variety of organ systems thought to play key roles in blood pressure homeostasis, including the heart, kidney, blood vessels, adrenal glands, and cardiovascular control centers in the brain[5]. In the brain, intraventricular injection of Angiotensin II causes a dramatic pressor response that is mediated by AT1A receptors[6].

In mice, AT1 receptors in the kidney are primarily responsible for the actions of Angiotensin II to cause hypertension[7]. Angiotensin II induction of NETosis in vitro via ROS/ peptidyl arginine deiminase type 4 and autophagy dependent pathways In EH patients initiated with Angiotensin II receptor blockers, circulating NETs and thrombin production levels were significantly reduced, whereas their plasma was unable to trigger procoagulant NETs [9].