Angiotensin II human acetate

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

Key Factor: Blood pressure ↑ on day 7, blood pressure in male was greater than in female.

Angiotensin II human acetate activates receptors: Ang II exerts its biological effects primarily by binding to its specific receptor AT1R. Once AT1R is activated, it can trigger various downstream signaling pathways;- Intracellular signaling pathways: The activation of AT1R initiates several intracellular signaling cascades, such as the activation of phospholipase C (PLC), protein kinase C (PKC), and the phosphorylation of members of the mitogen-activated protein kinase (MAPKs) family. These signaling pathways work together to promote the proliferation of cardiac myocytes and protein synthesis, leading to cardiac hypertrophy;- Inflammatory response: Ang II can promote the production of inflammatory factors like tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), which can further exacerbate myocardial injury and the fibrosis process;- Oxidative stress: Ang II can stimulate the generation of reactive oxygen species (ROS), and excessive ROS can not only directly damage cardiac myocytes but also activate transcription factors like NF-κB, enhancing the inflammatory response and cell apoptosis;- Extracellular matrix remodeling: Prolonged stimulation by Ang II leads to changes in extracellular matrix components, such as excessive deposition of collagen, which increases myocardial stiffness and disrupts normal heart function.

Mice: C57/BL6J male 8 wk old &bull
Administration: 2 μg/kg/min 4 weeks sc, osmotic pump implanted subcutaneously

Indicator changes: Blood pressure in WT mice increased significantly.
Appearance monitoring: cardiac hypertrophy and fibrosis.