Angiotensin II human (5 mL of 1 nM; intraperitoneal injection; 200-250 g Sprague-Dawley rats) acetate induces significant neutrophil recruitment that peaks at 4 hours and resolves by 24 hours ^[4].

To identify the AT1 receptor population critical for the development of hypertension, osmotic minipumps are implanted subcutaneously into each animal to continuously infuse Angiotensin II human (1000 ng/kg/min) acetate for 4 weeks. This treatment induces hypertension by activating AT1 receptors in the kidneys, promoting sodium reabsorption ^[5].

The primary actions of Angiotensin II human acetate are mediated by AT1 receptors, with AT2 receptors also contributing to blood pressure and renal function regulation ^[1].

Angiotensin II human acetate elevates blood pressure through various mechanisms, notably vasoconstriction, stimulation of the sympathetic nervous system, increased aldosterone production, and renal effects. Additional effects of Angiotensin II human acetate include stimulating the growth and migration of vascular smooth muscle cells, enhancing the synthesis of collagen types I and III in fibroblasts, leading to thickening of the vascular walls and myocardium, and causing fibrosis. These effects are primarily mediated by type 1 Ang II receptors (AT1) ^[2].

Angiotensin II (1 nM) promotes the expression of LOX-1 and VEGF, enhancing capillary formation in human coronary endothelial cells in a Matrigel assay. The effects related to Angiotensin II, including LOX-1 and VEGF expression, capillary formation, the generation of intracellular reactive oxygen species, 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].