Angiotensin II , human

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 (3-8), human (TFA), is an angiotensin AT1 receptor agonist with reduced activity.

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

Angiotensin II is a major biologically active vasoconstrictor peptide that regulates blood pressure by binding to AT1R and AT2R receptors. It stimulates the sympathetic nervous system, promotes aldosterone synthesis, and enhances renal function. Additionally, it induces vascular smooth muscle cell proliferation and increases collagen synthesis, leading to vascular and myocardial hypertrophy and fibrosis. It also promotes apoptosis and endothelial capillary formation. Angiotensin II is commonly used to induce hypertension and cardiac hypertrophy animal models.

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.

CAY10434 is an active inhibitor of CYP4A hydroxylase with an IC50 value of 8.8 nM in human kidney microsomal test. The maximum contractile value (Emax) of CAY 10434 was 6764 mg in improving the contractile process of angiotensin II.

Angiotensin I-13C6,15N (human, mouse, rat) TFA is a labeled version of Angiotensin I, using isotopes 13C and 15N, specifically targeted for human, mouse, and rat studies. This compound serves as a precursor to angiotensin II, which is formed through the cleavage by angiotensin-converting enzyme (ACE).

Eprosartan (SKF-108566J free base) is a selective, competitive nonpeptide angiotensin II receptor antagonist with high affinity for AT1 receptor subtypes, used as an antihypertensive agent. It exhibits inhibitory effects on angiotensin II receptors with IC50 values of 9.2 nM in rat adrenocortical membranes and 3.9 nM in human adrenocortical membranes.

Losartan Carboxylic Acid (E-3174), a potent AT1 antagonist (Kis: 0.57 nM, rat; 0.67 nM, human), produces a depressor response and vasodilatation. As a metabolite of losartan, it is more potent than losartan in blocking angiotensin II-induced responses in vascular smooth muscle cells.

4-hydroxy Valsartan is a major metabolite of the angiotensin II type 1 (AT1) receptor antagonist valsartan . It reduces platelet aggregation induced by epinephrine and collagen but not ADP in human whole blood.

Telmisartan acyl-β-D-glucuronide is a major metabolite of the angiotensin II receptor antagonist telmisartan . It does not bind human serum albumin and is cleared from rat plasma with a clearance rate of 180 ml/min/kg following intravenous administration.

Prostaglandin A1 (PGA1) was first isolated as a dehydration product of the PGE1 compounds found in human semen. 15-keto PGA1 is a metabolite of PGA1, produced by 15-hydroxy PG dehydrogenase. It can be produced from PGA1 in pig lung, trachea, aorta, and pulmonary artery tissue preparations. 15-keto PGA1, given at a concentration of 6 μM, causes vasoconstriction of rabbit lung that is comparable to that induced by angiotensin II.

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

AT2R antagonist 1 is a highly selective and potent AT2R (angiotensin II AT2 receptor) ligand.AT2R antagonist 1 has a high affinity for AT2R affinity (Ki: 29 nM).AT2R antagonist 1 inhibits common drug metabolizing CYP enzymes and has high stability in human, rat, and mouse liver microsomes.AT2R antagonist 1 has a high affinity for AT2R affinity (Ki: 29 nM).AT2R antagonist 1 has a high affinity for AT2R affinity (Ki: 29 nM). It has high stability in human, rat and mouse liver microsomes.

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

Safflor Yellow B mitigates angiotensin II-induced injury in human umbilical vein cells by modulating Bcl-2/p22(phox) expression and demonstrates neuroprotective effects [1].

18-Hydroxy-11-deoxy Corticosterone (18-OH-DOC) is a mineralocorticoid produced by the zona fasciculata of the adrenal gland, with its biosynthesis regulated by adrenocorticotropic hormone (ACTH) and angiotensin II. This regulation heightens 18-OH-DOC production in isolated human adrenal glomerulosa cells and allows for its formation from 11-deoxy corticosterone (DOC) in human SK-MEL188 melanoma cells. As an intermediate in progesterone metabolism, 18-OH-DOC can be converted to aldosterone in rat adrenal glands' capsular portion. Its continuous infusion (200 μg/rat per day) has been shown to raise systolic blood pressure in uninephrectomized saline-drinking rats, and elevated plasma levels of 18-OH-DOC have been observed in the adb/db mouse model of type 2 diabetes.

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.