Characterization of a murine model of endothelial dysfunction induced by chronic intraperitoneal administration of angiotensin II

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 TNF alpha, IL1 beta, IL17A, IL4, TGF beta, 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.

Automated summary

This study characterized a murine model of endothelial dysfunction induced by chronic intraperitoneal administration of angiotensin II (AGII) for 10 weeks, which led to increased production of systemic soluble VCAM, ROS, and ICAM-1 expression, as well as inflammation in the kidney, elevated blood pressure levels, vascular remodeling, and damage to various target organs. The proposed model is representative of ED and is easy to implement, safe, rapid, and inexpensive.