For the treatment of hypertension. It may be used alone or in combination with thiazide diuretics.
Benazeprilat, the active metabolite of Benazepril, competes with angiotensin I for binding at the angiotensin-converting enzyme, blocking the conversion of angiotensin I to angiotensin II. Inhibition of ACE results in decreased plasma angiotensin II. As angiotensin II is a vasoconstrictor and a negative-feedback mediator for renin activity, lower concentrations result in a decrease in blood pressure and stimulation of baroreceptor reflex mechanisms, which leads to decreased vasopressor activity and to decreased aldosterone secretion. Benazeprilat may also act on kininase II, an enzyme identical to ACE that degrades the vasodilator bradykinin.
Most likely symptom of overdosage is severe hypotension. Most common adverse effects include headache, dizziness, fatigue, somnolence, postural dizziness, nausea, and cough.
Peak in plasma within 0.5-1.0 hours. The extent of absorption is at least 37% as determined by urinary recovery and is not significantly influenced by the presence of food in the GI tract.
10-11 hours
Benazepril and benazeprilat are cleared predominantly by renal excretion in healthy subjects with normal renal function. Nonrenal (i.e., biliary) excretion accounts for approximately 11%-12% of benazeprilat excretion in healthy subjects.
* 0.35 L/hr/kg [pediatric hypertensive patients receiving multiple daily doses of Benazepril hydrochloride 0.1 - 0.5 mg/kg] * 0.13 L/hr/kg [healthy adults receiving a single dose of 10 mg]