Sigma-Aldrich Angiotensin Ii Human - Cas

Research area: Cell signaling

Cell permeable: no

Primary Target adenylate cyclase activity

Product does not compete with ATP.

Reversible: no

Angiotensin II, Human has been used to induce fibrosis in mice to evaluate the impact of fibroblast loss on cardiac function after injury.[1] It has also been used to induce abdominal aortic aneurysm (AAA) progression in mice.[2]

Angiotensin II is a crucial component of the Renin-Angiotensin System (RAS). It plays a vital role in vasoconstriction, regulating blood pressure, and controlling fluid balance by influencing the retention of sodium and water in the renal tubules. Furthermore, Angiotensin II stimulates the release of aldosterone from the adrenal gland, contributing to the maintenance of fluid and electrolyte balance regulation. Angiotensin II also promotes inflammation and tissue injury.[3] It Inhibits adenylate cyclase activity in spontaneously hypertensive rats.[4] Angiotensin II also activates JAK2 in smooth muscle cells, as well as several kinases including p125FAK, cytosolic calcium-dependent tyrosine kinase, and p60c-src in various cell types. In vascular smooth muscle cells, it activates ERK1/2, JNK, and p38 MAP Kinase.[5]

Yes

Toxicity: Standard Handling (A)

H-Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-OH

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 1 week at 4°C or for up to 1 month at -20°C.

Zhu, M., et Al. 2000. J. Neurophysiol.84, 2494.
Natarajan, R., et Al. 1999. Hypertension 33, 378.
Mazzolai, L., et Al. 1998. Hypertension 31, 1324.
Earp, H.S., et Al. 1995. J. Biol. Chem. 270, 28440.
Ishida, M., et Al. 1995. Circ. Res. 77, 1053.
Vyas, S.J., and Jackson, E.K. 1995. J. Pharmacol. Exp. Ther. 273, 768.

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