Table 1.

Describes pharmacological characteristics of the three classes of anti-RAAS agents: ACE inhibitors (ACEi), direct renin inhibitors and angiotensin receptor blockers (ARBs). Based on their different mechanism of action, these classes of drugs are used for different treatment, even if the risk of main adverse effects is similar for all the categories.

Classes of drugs	Mechanism of action	Indications	Half-life	Bradichinine accumulation	Impact on plasma renin concentration and activity	Main adverse effects
Angiotensin converting enzyme inhibitors (ACEi)	RAAS down-regulation by inhibition of the ACE enzyme activity, which converts Angiotensin I in Angiotensin II	Treatment of hypertension, heart failure, chronic non-diabetic and diabetic renal disease, dry cough	2–40 h	Yes	↑ Renin concentration ↔ Renin activity	Increased risk of hypotension, AKI, hyperkalemia, angioedema
Direct Renin Inhibitors (DRI)	RAAS down-regulation by PRA reduction and inhibition of Angiotensinogen conversion to Ang I	Treatment of hypertension	24 h	No	↑ Renin concentration ↓ Renin activity	Dizziness, headache, muscle or joint aches, hyperkalemia, AKI
Angiotensin 1 receptor blockers (ARBs)	Blockage of Angiotensin II binding to its receptor (AT1R)	Treatment of hypertension, heart failure, chronic non-diabetic and diabetic renal disease	6–24 h	No	↑ Renin concentration ↔ Renin activity	Increased risk of hypotension, AKI, hyperkalemia

ACEi: angiotensin-converting enzyme inhibitors; RAAS: renin–angiotensin–aldosterone system; ACE: angiotensin-converting enzyme; AKI: acute kidney injury; DRI: direct renin inhibitors; PRA: plasma renin activity; Ang I: angiotensin I; ARBs: angiotensin receptor blockers; AT1R: angiotensin type 1 receptor.