Angiotensin II is used in animal modeling to construct cardiovascular and cerebrovascular disease models. Angiotensin II (5 mL of 1 nM; intraperitoneal injection; 200-250 g Sprague-Dawley rats) induces significant neutrophil recruitment that peaks at 4 hours and resolves by 24 hours ^[4].

To study the critical role of AT1 receptors in the pathogenesis of hypertension, osmotic minipumps are surgically implanted subcutaneously into each animal to continuously infuse Angiotensin II (1000 ng/kg/min) for 4 weeks. Angiotensin II causes hypertension primarily by activating AT1 receptors in the kidney, which promote sodium reabsorption ^[5].

Most actions of Angiotensin II are mediated by AT1 receptors, though AT2 receptors also contribute to blood pressure and renal function regulation ^[1]. Angiotensin II raises blood pressure by mechanisms including vasoconstriction and stimulation of the sympathetic nervous system, alongside its cellular effects on vascular smooth muscle cells and fibroblasts. These actions result in structural changes within the vascular wall and myocardium, mediated primarily through AT1 receptors ^[2].

Angiotensin II raises blood pressure through several mechanisms, notably vasoconstriction, stimulation of the sympathetic nervous system, increased aldosterone biosynthesis, and renal effects. Other actions of Angiotensin II include promoting the growth, migration, and mitosis of vascular smooth muscle cells, as well as increasing collagen type I and III synthesis in fibroblasts, leading to vascular wall and myocardial thickening and fibrosis, primarily mediated by type 1 Ang II receptors (AT1) ^[2].

Angiotensin II (1 nM) stimulates the expression of LOX-1 and VEGF and enhances capillary formation from human coronary endothelial cells in Matrigel assays. The effects mediated by Angiotensin II on LOX-1 and VEGF expression, capillary formation, intracellular reactive oxygen species generation, and phosphorylation of p38 and p44/42 mitogen-activated protein kinases are inhibited by the anti-LOX-1 antibody, the NADPH oxidase inhibitor apocynin, and the Ang II type 1 receptor blocker Losartan, but not by the Ang II type 2 receptor blocker PD123319 ^[3].