Chronic intraperitoneal administration of angiotensin II significantly increased plasma VCAM levels (24.5 vs. 10.8 pg/mL) and induced endothelial dysfunction, oxidative stress, and hypertension.
Chronic intraperitoneal administration of angiotensin II provides a viable, inexpensive murine model for studying endothelial dysfunction and its associated cardiovascular and organ complications.
Absolute Event Rate: 24.5% vs 10.8%
p-value: p=<0.0001
Endothelial dysfunction (ED) is a key factor for the development of cardiovascular diseases. Due to its chronic, life-threatening nature, ED only can be studied experimentally in animal models. Therefore, this work was aimed to characterize a murine model of ED induced by a daily intraperitoneal administration of angiotensin II (AGII) for 10 weeks. Oxidative stress, inflammation, vascular remodeling, hypertension, and damage to various target organs were evaluated in treated animals. The results indicated that a chronic intraperitoneal administration of AGII increases the production of systemic soluble VCAM, ROS and ICAM-1 expression, and the production of TNFα, IL1β, IL17A, IL4, TGFβ, and IL10 in the kidney, as well as blood pressure levels; it also promotes vascular remodeling and induces non-alcoholic fatty liver disease, glomerulosclerosis, and proliferative retinopathy. Therefore, the model herein proposed can be a representative model for ED; additionally, it is easy to implement, safe, rapid, and inexpensive.
Trejo-Moreno et al. (Wed,) conducted a other in Endothelial dysfunction (n=37). Angiotensin II vs. Isotonic saline solution was evaluated on Plasma soluble VCAM levels (pg/mL) (p=<0.0001). Chronic intraperitoneal administration of angiotensin II significantly increased plasma VCAM levels (24.5 vs. 10.8 pg/mL) and induced endothelial dysfunction, oxidative stress, and hypertension.