ACE, a homologue of ACE 2, converts Ang I into Ang II.  ACE increases the amount of Ang II, a vasoconstrictor, and decreases the amount of a vasodilator.  This consequently results in increased blood pressure.  A class of drugs called ACE inhibitors, which are used for treating symptoms such as high blood pressure, block the activity of ACE.  ACE is generally more expressed than its homologue ACE 2.  

Angiotensin-converting enzyme (ACE)

ACE2 is a homologue of ACE.  Both enzymes are carboxypeptidases, meaning they cleave amino acids from the c-terminal of the peptide.  However, these homologues cleave the amino acid sequences at different points which leads to their different products.  ACE2 has four main physiological roles:

- Regulating blood pressure via its role in the renin-angiotensin-aldosterone system (RAAS)

- Limiting the amount of ACE substrate by converting Ang I into Ang 1-9

- Degrading Ang II in order to minimize its harmful effects

- Forming Ang 1-7 in order to maximize its cardioprotective effects

Angiotensin-converting enzyme 2 (ACE2)

Ang I is cleaved by angiotensin-converting enzyme (ACE) to form angiotensin II (Ang II).  This product is the main effector molecule that regulates the RAS system.  Endopeptidases and oligopeptidases can likewise cleave Ang I to form angiotensin (1-7).  This product works against Ang II.  

Michigan State University

Renin is an enzyme that is synthesized in the kidneys in an inactive form.  It is secreted into the blood stream and becomes activated when sodium levels drop, when hypotension is detected, and during sympathetic activation.  It goes on to cleave angiotensinogen to form angiotensin I (Ang I).  

Renin

Muñoz-Durango, N., Fuentes, C. A., Castillo, A. E., González-Gómez, L. M., Vecchiola, A., Fardella, C. E., & Kalergis, A. M. (2016). Role of the renin-angiotensin-aldosterone system beyond blood pressure regulation: molecular and cellular mechanisms involved in end-organ damage during arterial hypertension. International Journal of Molecular Sciences, 17(7), 797.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964362/pdf/ijms-17-00797.pdf

Role of the Renin-Angiotensin-Aldosterone System beyond Blood Pressure Regulation: Molecular and Cellular Mechanisms Involved in End-Organ Damage during Arterial Hypertension

Learn Before

Related

Learn After