Angiotensin II human acetate (Angiotensin II acetate) is a vasoconstrictor that mainly acts on the AT1 receptor. It stimulates sympathetic nervous stimulation and increases aldosterone biosynthesis and renal actions. It also induces the growth of vascular smooth muscle cells. It increases collagen type I and III synthesis in fibroblasts, weakening the vascular wall, myocardium, and fibrosis. Angiotensin II human acetate also induces apoptosis.
Most of the known actions of Angiotensin II (Ang II) human acetate are mediated by AT1 receptors; the AT2 receptor regulates blood pressure and renal function.
Angiotensin II human acetate raises blood pressure (BP) through several actions, the most important ones being vasoconstriction, sympathetic nervous stimulation, increased aldosterone biosynthesis, and renal actions. Other Angiotensin II human acetate actions include induction of growth, cell migration, and mitosis of vascular smooth muscle cells, increased synthesis of collagen type I and III in fibroblasts, leading to thickening of the vascular wall and myocardium, and fibrosis. These actions are mediated by type 1 Ang II receptors (AT1).
Angiotensin II (1 nM) induces the expression of LOX-1 and VEGF and enhances capillary formation from human coronary endothelial cells in Matrigel assay. Angiotensin II -mediated expression of LOX-1 and VEGF, capillary formation, intracellular reactive oxygen species generation, and phosphorylation of p38 as well as p44/42 mitogen-activated protein kinases were suppressed by anti-LOX-1 antibody, nicotinamide-adenine dinucleotide phosphate oxidase inhibitor apocynin and the Ang II type 1 receptor blocker Losartan, but not by the Ang II type 2 receptor blocker PD123319.
