Renin is an aspartyl protease that raises blood pressure, retains sodium, and alters gene transcription to adversely affect the kidney and heart. Renin cleaves a decapeptide, angiotensin I, from a large hepatic protein, angiotensinogen. Angiotensin-converting enzyme activates angiotensin I to the octapeptide, angiotensin II, by removal of two amino acids from the carboxyl terminus. Angiotensin II interacts with AT1 receptors to mediate most renin effects. The system is involved with the pathology of the following: congestive heart failure, myocardial infarction, hypertension, and diabetes mellitus (renal damage). Inhibitors of the system are beneficial in treating these pathologies and include direct renin inhibitors, angiotensin-converting enzyme inhibitors, and angiotensin receptor antagonists.
The renin-angiotensin system is thought to be important in adaptations to low-salt diets and normal development of the kidneys in utero.