Quinapril is an angiotensin-converting enzyme (ACE) inhibitor that was developed in the 1980s and was approved by the FDA, in 1989, for the treatment of hypertension.[1] In this study, researchers determined that quinapril had a lower incidence of adverse events as compared to other ACE inhibitors like captopril and enalapril, as well as the thiazide diuretic, chlorthalidone.[1] Quinapril has demonstrated effectiveness in lowering systolic blood pressure by 13 mm Hg and diastolic blood pressure by 10 mm Hg in approximately two out of three individuals.[2][3][4]

Quinapril has also had non-approved FDA indications for chronic heart failure (CHF) and slowing the progression of renal disease in diabetic patients. According to the SOLVD trial, ACE inhibitors, as a class, have shown to be beneficial in chronic heart failure (CHF).[5] The primary therapeutic effects include reduction of heart failure hospitalizations, hospitalizations for any reason, and risk of death. Additionally, the HOPE trial found that patients taking ACE inhibitors reduce the risk of ischemic stroke, non-fatal myocardial infarction, and cardiovascular death.[6] As a class, ACE inhibitors have shown to reduce proteinuria in diabetic patients. More importantly, however, research has demonstrated quinapril to be an agent that reduced microalbuminuria in essential hypertension and diabetic patients without significantly affecting insulin effectiveness or lipid levels.[7]

Quinapril is a non-sulphylhydryl ACE inhibitor that acts by blocking the action of ACE, which plays a vital role in the renin-angiotensin-aldosterone system (RAAS). Quinapril is metabolized into quinaprilat in the liver, from where the drug enters the circulation. After conversion, the liver releases quinaprilat into the peripheral circulation where it inhibits ACE; the enzyme is responsible for the conversion of angiotensin I to angiotensin II. Angiotensin II is the hormone that promotes the stimulation of the hormone aldosterone, which is responsible for salt and water retention.[8] A combination of salt and water retention, coupled with peripheral vasculature constriction, leads to the development of systemic hypertension. Quinapril (and its metabolite quinaprilat) decreases systemic (peripheral and renal) vascular resistance, thereby decreasing blood pressure. Distribution is widespread, except for brain tissue.[9] The renal system clears the majority of quinapril, and the maximum observable effect of ACE inhibitors takes place at 5 hours.[4][10]

The administration of quinapril is via the oral route. Plasma clearance of quinapril correlates to the creatinine clearance of a patient. The dosing range that researchers tested was between 0.625 to 80 mg orally once daily, but the most effective antihypertensive effects were noted at doses of 20 mg orally once daily.[3] Patients with mild to moderate hypertension should be initiated on a dose range between 5 and 40 mg orally once daily. In patients with renal impairment, doses should be reduced to between 2.5 and 20 mg orally once daily.[11] Interestingly, twice daily dosing has been noted to achieve a more significant blood pressure trough effect in hypertensive patients as opposed to a similar total dose administered daily. 

Adverse effects of quinapril include dry cough (as is typical among all ACE inhibitor class members), hyperkalemia, angioedema, dizziness, hypotension, and renal dysfunction.[12][13][14] Less common adverse effects include skin rash and dysgeusia.[14]

Angioedema is a rare but well-documented side effect of ACE inhibitors, which often presents as facial, tongue, and lip swelling. However, there may be unique instances when patients present with isolated swelling of the small bowel. This presentation, also called intestinal-type angioedema, may manifest in patients taking ACE inhibitors that present with abdominal pain, nausea, vomiting, and/or diarrhea.[15]

ACE inhibitors, including quinapril, are contraindicated in pregnancy since they counteract the RAAS, which is essential for fetal renal development.[14] Possible complications of use of quinapril in pregnancy may include but are not limited to fetal lung hypoplasia, fetal renal hypoplasia/failure, oligohydramnios, skeletal hypoplasia, hypotension, and death.

Quinapril is also contraindicated in patients presenting with hyperkalemia, history, or current presentation of angioedema (regardless of the ACE inhibitor used), bilateral renal artery stenosis, acute kidney injury leading to renal failure with prior ACE inhibitor use, and aliskiren use within the last 36 hours. 

Although there was one report of agranulocytosis in a neutropenic patient using quinapril, there are no other reports of agranulocytosis noted in the literature, as has been found in rare cases of captopril use, one of the original ACE inhibitors.