Angiotensin II human acetate can induce blood vessel constriction: After Ang II binds to its receptor (primarily the AT1 receptor), it activates a series of signaling pathways, such as the opening of calcium channels, leading to an increase in intracellular calcium concentration in vascular smooth muscle cells, causing them to contract, which in turn raises blood pressure;-
Promoting inflammatory response: Ang II can also promote the production of inflammatory mediators, for example, by activating NADPH oxidase to produce excessive reactive oxygen species (ROS). These ROS can damage endothelial cells and promote the infiltration of inflammatory cells, resulting in thickening and hardening of the blood vessel walls, further exacerbating the development of hypertension;-
Fibrosis and remodeling: Long-term exposure to high levels of Ang II leads to structural changes in the heart and blood vessels, including myocardial hypertrophy, ventricular remodeling, and fibrosis of the blood vessel walls, all of which are important pathological foundations for hypertension and its complications;-
Dysregulation of water and sodium metabolism: As mentioned earlier, Ang II stimulates the adrenal cortex to secrete aldosterone, increasing sodium reabsorption in the kidneys, leading to water and sodium retention in the body, increasing blood volume, which raises blood pressure;-
Neuroendocrine regulation: Ang II also plays a role in the regulation of the neuroendocrine system, such as influencing the activity of the sympathetic nervous system, enhancing its excitatory effects on the cardiovascular system, indirectly leading to increased blood pressure.
Mice: C57/BL6J ? male and female ? 12-16 wk old ? 21-27 g
Administration: 800 ng/kg/min, 0.003 mL/min ? 7 days ? sc, osmotic pump implanted subcutaneously
Note
Effect of gender: Chronic ANG II-induced hypertension differs by gender in awake mice. Female mice may be protected from the ANG II-induced increase in blood pressure.