Background:

Angiotensin III (Asp | Arg-Val-Tyr-Ile-His-Pro-Phe) is a hexapeptide formed as a result of a cleavage at the N-terminus of Angiotensin II, a key factor in the Renin-Angiotensin-Aldosterone (RAAS) system by angiotensinases located in red blood cells and the vascular beds of most tissues. It has 40% of the presser activity of angiotensin II, but 100% of the aldosterone-producing activity.

In peripheral Ang systems, Ang II is the main effector peptide in the systemic circulation, although exogenous Ang III can be as potent as Ang II in, for example, stimulating aldosterone secretion [1] or inhibiting renin release [2]. In the rat brain, Ang III was found to be equipotent with Ang II as a pressor agent or dipsogen [3] and was bound as avidly to the nervous system as Ang II. Ang receptor subtype AT1 has greater affinity towards Ang II and is also responsive to Ang III, while the AT2 receptor subtype appears to be more sensitive to Ang III but less responsive to Ang II [4].

参考文献:
1. Blair-West, JR. et al. (1980) J. Endocrinol. 87, 409.
2. Fei, DTW. et al. (1980) Life Sci. 27, 1495.
3. Fink, GD. et al. (1985) Am. J. Physiol. Endocrinol. Metab. 249, E201.
4. Wright, JW. et al. (2011) Prog. Neurobiol. 95, 49.