Trade Names:Lotensin- Tablets 5 mg- Tablets 10 mg- Tablets 20 mg- Tablets 40 mg
Competitively inhibits angiotensin-converting enzyme (ACE), resulting in decreased conversion of angiotensin I to angiotensin II, a potent vasoconstrictor that stimulates aldosterone secretion. Results in decreased vasopressor activity and decreased aldosterone secretion.
T max is 0.5 to 1 h (benazepril), 1 to 2 h (benazeprilat) in fasting state, and 2 to 4 h (benazeprilat) in nonfasting state. Up to 37% absorbed.
Protein binding is about 96.7% (benazepril) and about 95.3% (benazeprilat).
Converted to benazeprilat (active) by cleavage of ester group (primarily in liver). Also metabolized to glucuronide conjugates.
Benazepril (trace amounts), benazeprilat (about 20%), benazepril glucuronide (4%), benazeprilat glucuronide (8%).Nonrenal (eg, biliary)
About 11% to 12% (benazeprilat).
Within 1 h.
2 to 4 h.
In those with Ccr up to 30 mL/min, peak benzaprilat levels and initial t ½ increase and time to steady state may be delayed.
Treatment of hypertension.
Hypersensitivity to ACE inhibitors.
PO 10 mg/day for patients not receiving a diuretic. In patients taking diuretics that cannot be discontinued, give initial dose of 5 mg. Administer without regard to meals or with food if GI upset occurs.Maintenance
PO 20 to 40 mg/day as single dose or in 2 divided doses; doses up to 80 mg have been used.Children (6 yr of age and older) Initial dose
PO 0.2 mg/kg/day.Maintenance
PO 0.2 to 0.6 mg/kg as single dose; doses above 0.6 mg/kg (or more than 40 mg) have not been studied.Renal function impairment
Initial dose is 5 mg/day for patients with Ccr less than 30 mL/min. Dosage may be titrated upward until BP is controlled or to a total max dose of 40 mg/day.
For patient who cannot swallow tablets or whose calculated dose (mg/kg) does not correspond to available tablet size, use extemporaneous suspension as follows: to prepare 150 mL of 2 mg/mL suspension, add 75 mL Ora-Plus oral suspending vehicle to amber polyethylene terephthalate (PET) bottle containing 15 benazepril 20 mg tablets and shake for at least 2 min. Let stand for 1 h minimum then shake for minimum of 1 additional min, add 75 mL of Ora-Sweet oral syrup and shake to disperse ingredients.
Shake suspension before measuring dose. Measure and administer prescribed dose using dosing syringe, dosing spoon, or dosing cup.
Store tablets at or below 86°F. Protect from moisture. Store suspension in refrigerator (36° to 46°F). Discard any unused suspension after 30 days.
May decrease bioavailability of benazepril; separate administration by 1 to 2 h.Diuretics
May cause symptomatic hypotension after initial dose of benazepril.Lithium
May increase lithium levels and symptoms of lithium toxicity.Potassium preparations, potassium-sparing diuretics
May increase serum potassium levels.Salicylates (eg, aspirin)
May reduce effects of benazepril, especially in low-renin or volume-dependent hypertensive patients.
None well documented.
Angina pectoris, ECG changes, palpitations, peripheral edema, postural hypotension, symptomatic hypotension, syncope (postmarketing).
Headache (6%); dizziness (4%); fatigue, postural dizziness, somnolence (2%); anxiety, asthenia, decreased libido, hypertonia, insomnia, nervousness, paresthesia (postmarketing).
Alopecia, apparent hypersensitivity (dermatitis, pruritus, rash), flushing, pemphigus, photosensitivity, Stevens-Johnson syndrome, sweating (postmarketing).
Nausea (1%); constipation, gastritis, melena, pancreatitis, vomiting (postmarketing).
Impotence, increased BUN, increased serum creatinine, UTI (postmarketing).
Eosinophilia, hemolytic anemia, leukopenia, thrombocytopenia (postmarketing).
Increased serum creatinine (2%); hyperkalemia, increased uric acid, increased blood glucose, increased serum bilirubin, increased liver enzymes (postmarketing).
Arthralgia, arthritis, myalgia (postmarketing).
Protein uria (postmarketing).
Chronic dry cough (1%); asthma, bronchitis, eosinophilic pneumonitis, sinusitis (postmarketing).
Anaphylactoid reactions; angioedema; fetal and neonatal morbidity and death, hyponatremia, infection (postmarketing).
When used in pregnancy during the second and third trimesters, ACE inhibitors can cause injury and even death to the developing fetus. When pregnancy is detected, discontinue therapy as soon as possible.
Ensure serum electrolytes and renal function are monitored periodically. Monitor and record BP and pulse. Monitor WBC in patients with collagen-vascular disease.
Category D (second and third trimester); Category C (first trimester). When pregnancy is detected, discontinue ACE inhibitors as soon as possible.
Excreted in breast milk; avoid use in breast-feeding mothers if possible.
Not recommended in children younger than 6 yr of age or if glomerular filtration rate is less than 30 mL/min.
Consider lower starting dose and slower dose titration.
Reduce dose. Monitor renal function during first few weeks of therapy, when dose is increased, or during concurrent treatment with diuretic. Benazepril dose reduction or discontinuation of diuretic may be required if increases in Ccr and BUN occur.
May cause drowsiness, dizziness, or lightheadedness. Use with caution while driving or performing other tasks requiring mental alertness until tolerance is determined.
May occur. Use with extreme caution in patients with hereditary angioedema. Angioedema of the tongue, glottis, or larynx may cause airway obstruction; consider use of subcutaneous epinephrine. Consider intestinal angioedema in differential diagnosis of patients on ACE inhibitor presenting with abdominal pain.
If possible, discontinue diuretic therapy for 2 to 3 days prior to beginning benazepril therapy.
Persistent nonproductive cough, always resolving after discontinuation of therapy, has been reported with ACE inhibitors.
May occur. Discontinue benazepril as soon as possible if patient becomes pregnant.
ACE inhibitors rarely have been associated with a syndrome that starts with cholestatic jaundice and progresses to fulminant hepatic necrosis and sometimes death.
Has been reported. Risk factors include renal function impairment, diabetes mellitus, and concomitant use of potassium-sparing diuretics, potassium supplements, and/or potassium-containing salt substitutes.
Significant decreases in BP may occur after first dose, especially in severely salt- or volume-depleted patients (eg, those undergoing dialysis or vigorous diuretic therapy) or those with heart failure. Risk is minimized by discontinuing use of diuretics, increasing salt intake about 1 wk before initiating benazepril, or decreasing benazepril dose.
Has occurred with other ACE inhibitors, most often in patients with renal function impairment and a collagen-vascular disease (eg, systemic lupus erythematosus).
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