Angiotensin II , human

Angiotensin II (3-8), human, is a less effective agonist at the angiotensin AT1 receptor.

Angiotensin II (5-8) is an endogenous C-terminal fragment of the peptide vasoconstrictor angiotensin II

Angiotensin II is a potent direct vasoconstrictor, causing arteries and veins to constrict, so leading to an increase in blood pressure. Angiotensin also potentiates the release of norepinephrine by a direct action on postganglionic sympathetic fibers.

Angiotensin II human acetate is a key vasoconstrictor peptide in the renin-angiotensin system. It regulates blood pressure by binding to AT1R and AT2R receptors, stimulates the sympathetic nervous system, promotes aldosterone synthesis and renal function, induces vascular smooth muscle cell proliferation and collagen synthesis, leading to vascular and myocardial hypertrophy and fibrosis, while also promoting apoptosis and endothelial capillary formation. It is commonly used to induce hypertension and cardiac hypertrophy models.

Angiotensin II human TFA is a potent vasoconstrictor in the renin-angiotensin system that regulates blood pressure through interactions with AT1R and AT2R receptors. It activates sympathetic nerve activity, promotes aldosterone synthesis and renal function, induces proliferation of vascular smooth muscle cells, and enhances type I and III collagen production in fibroblasts, leading to vascular and myocardial thickening and fibrosis. It also triggers apoptosis and promotes capillary formation, making it suitable for establishing models of cardiac hypertrophy, hypertension, and abdominal aortic aneurysm.

Angiotensin II is a potent direct vasoconstrictor, causing arteries and veins to constrict, so leading to an increase in blood pressure.

Angiotensin III, human, mouse (Angiotensin III, human, mouse(3TFA))(3TFA) is an endogenous angiotensin II receptor (AT2R) agonist(IC50s of 0.648 nM).

Angiotensin I (human, mouse, rat) is the precursor to the vasoconstrictor peptide angiotensin II, cleaved by the angiotensin-converting enzyme (ACE). This peptide hormone causes vasoconstriction and increases blood pressure as part of the renin–angiotensin system, also stimulating aldosterone release from the adrenal cortex to promote sodium retention by the kidneys.