Angiotensin-converting-enzyme inhibitors are a phmaceutical drugs used to treat several diseases such as hypertension and heart failure. During the passage of vessels in the lungs and renal vasculature, Ang I is generated by the action of renin on angiotensinogen which is then converted into Ang II by the action of an exopeptidase called ACE (Peter R et al., 1983). This is where ACE inhibitors comes into actions blocking the conversion of Ang I to Ang II. This conversion can be inhibited by angiotensin-converting enzyme inhibitors which results in vasodilation, decrease in blood volume which leads to a lower blood pressure and decrease in oxygen demand, reduction in Na retention and renin-angiotensin-aldosterone system activation (Chua D. et al., 2011). ACE inhibitors are categorised into two main groups, lower-affinity or plasma inhibitors and higher-affinity or tissue inhibitors. Some examples of ACE inhibitors include perindopril, quinapril, Ramipril, benazepril captopril, enalapril and Lisinopril (Krysiak R et al., 2008). Before administrating ACE inhibitors some precautions are required which include severe renal or cardiac failure, in case the patient is either hypovolemic or taking high- dose diuretic. Some indications of ACE inhibitors include hypertension, heart failure, and diabetes mellitus. Some contraindications include patients who have a history of hypersensitivity to any ACE inhibitor drugs or its components, angioedema, hypotension, pregnancy and current use of aliskiren in a patient with diabetes mellitus. Moreover, ACE inhibitors produce many beneficial effects, including regulation of smooth muscle cell proliferation and migration, anti-inflammatory, antioxidant effects and cytoprotection of vascular endothelium. Some of the adverse effects of ACE inhibitors include first-dose hypotension. Patients taking ACE inhibitors are more at risk for an abrupt fall in blood pressure after the first intake if they have high plasma renin before the treatment. Hyperkalaemia is another adverse effect which is defined a rise in plasma potassium after the intake of ACE inhibitor as a result of decrease in aldosterone secretion which in turn causes a decrease renal potassium excretion. ACE-induced angioedema has a low incidence of 0.1% to 0.2%, however, despite this its much feared due to its potentially life-threatening upper-airway obstruction most commonly in tongue or oropharynx (Vleeming W et al., 1998). Considering this, it is therefore of major importance that the physician is able to recognise these adverse effects, since a considerable percentage of patients are and will be under ACE inhibitor treatment