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The renin-angiotensin system (RAS) plays a key role in blood pressure regulation, fluid and electrolyte balance, cellular growth, thirst, and cardiac/renal function. The classic system primarily involves 2 enzymes: renin, which cleaves angiotensinogen to the inactive decapeptide angiotensin (Ang) I; and Ang-converting enzyme (ACE), a dipeptidyl carboxypeptidase that hydrolyzes Ang I to the octapeptide Ang II. The elucidation of the ACE pathway in parallel with potent and selective ACE inhibitors is clearly a pivotal achievement in our understanding of the RAS and in attaining effective therapies for hypertension and end organ damage. Indeed, ACE inhibitors attenuate Ang II formation and augment the levels of the heptapeptide Ang (1–7), a peptide that counterbalances the actions of Ang II on blood pressure and cellular growth through a unique receptor system. Ang II mediates the majority of its actions at the Ang II type 1 (AT1) receptor, including the stimulation of vasoconstriction, sodium retention, cellular growth, and oxidative stress, whereas recent studies show that Ang (1–7) at the AT1–7 or mas receptor and Ang II via the AT2 receptor subtype counterregulate the actions of Ang II at the AT1 receptor.The discovery of the ACE homolog ACE2 provides further evidence that the RAS is far more complex than originally thought. The enzymatic cascade of the RAS should now encompass the ACE2-dependent pathways that directly yield Ang (1–9) from Ang I and degrade Ang II to Ang (1–7) (Figure). The interplay between ACE and ACE2 that may govern the formation and metabolism of Ang effector peptides warrants the simultaneous study of both enzymes to ultimately assess their contribution to blood pressure regulation and cardiac/renal function. ACE/ACE2 contribution to the formation of angiotensin peptides. In the classic pathway, Ang I is converted by ACE to Ang II. Ang (1–7) can be …

Does the Angiotensin-Converting Enzyme (ACE)/ACE2 Balance Contribute to the Fate of Angiotensin Peptides in Programmed Hypertension?