Member of the RAS, produced from Ang-II by aspartyl aminopeptidase A (APA) and glutamyl APA
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Kopf and Campbell (2013) Endothelial Metabolism of Angiotensin II to Angiotensin III, not Angiotensin (1–7), Augments the Vasorelaxation Response in Adrenal Cortical Arteries. Endocrinology, 154(12) 4768 PMID: 24092640
Park et al (2013) Cardioprotective effects of angiotensin III against ischemic injury via the AT2 receptor and KATP channels. Physiol. Rep. 1(6) e00151 PMID: 24400153
Aspartyl aminopeptidase A (APA) and glutamyl APA, produce angiotensin III (Ang-III) by removing an aspartic acid from the N-terminal of angiotensin-II (Ang-II). Ang-III has many similar biological properties to Ang-II including aldosterone secretion and vasoconstriction, however some of its functions oppose those of Ang-II, such as sodium excretion and secretion of atrial natriuretic peptide (ANP). Due to its ability to promote ANP secretion Ang-III has some cardio protective effects.
Ang-III likely binds to both G-protein-coupled Ang-II type 1 (AT1) and Ang-II type 2 (AT2) receptors with a similar affinity to that of Ang-II. Ang-III appears to be cleared from the plasma at a faster rate than Ang-II, therefore the physiological effects of Ang-III are likely to limited to the site at which it is produced
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