benazepril (Lotensin)
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Introduction
Tradename: Lotensin.
Indications
- hypertension, especially in combination with diuretics
- congestive heart failure
- diabetic nephropathy
- scleroderma renal crisis
- nondiabetic proteinuric nephropathy[3]
Contraindications
Caution: elderly patient may have exaggerated response
Dosage
HTN. Start 10 mg PO QD, max 80 mg/day
Tabs: 5, 10, 20, 40 mg. Adjust for renal clearance < 30 mL/min
Pharmacokinetics
- 37% bioavailability, not affected by food
- extensive 1st pass metabolism in the liver, by hydrolysis to its active metabolite (benazeprilat), via enzymatic hydrolysis
- volume of distribution is 8-9 L
- protein binding 96.7%
- elimination 1/2life (benazeprilat):
- 22 hours initially
- 10-11 hours after after multiple dosing
- eliminated (benazeprilat) by kidney (11-12% by non renal metabolism)
- angiotensin converting enzyme (ACE)
- peak effect in 1-2 hours after oral administration (2-20 mg)
- > 90% inhibition of ACE for 24 hours after 5-20 mg dose
- blood pressure
- peak effect after 1 dose: 2-6 hours
- maximum effect 2 weeks
- 6% of benazeprilat eliminated after 4 hours of hemodialysis
elimination via liver
elimination via kidney
Monitor
K+, BUN, creatinine, WBC (see ACE inhibitor)
Adverse effects
- cardiovascular
- central nervous system
- skin: rash, pruritus, angioedema
- metabolic: hyperkalemia, hyponatremia
- gastrointestinal:
- genitourinary: impotence, decreased libido
- hematologic: neutropenia, eosinophilia
- neuromuscular:
- ocular: blurred vision
- hepatic: hepatitis
- renal: proteinuria, oliguria, azotemia, renal insufficiency
- respiratory:
- chronic cough
- non-productive
- persistent
- more often in women
- 5-29% of patients
- asthma, bronchitis, bronchospasm, dyspnea
- sinusitis
- chronic cough
- diaphoresis
- increased serum creatinine
- 15-20% initial increase is acceptable[5]; up to 30% acceptable[4]
- decline in creatinine within 1 month[5] (2 months[4]), otherwise discontinue
- drug adverse effects of renin-angiotensin-aldosterone system inhibitors (RAAS inhibitors)
- drug adverse effects of ACE inhibitors
- drug adverse effects of antihypertensive agents
Drug interactions
- benazepril & K+ sparing diuretics may increase risk of hyperkalemia
- non-steroidal anti-inflammatory drugs (NSAIDs) may reduce anti-hypertensive action of benazepril
- allopurinol & benazepril may increase risk of neutropenia
- antacids may diminish absorption of ACE inhibitors
- probenecid may increase serum levels of ACE inhibitors
- phenothiazines may increase ACE inhibitor effect
- rifampin may increase ACE inhibitor effect
- ACE inhibitors may increase serum digoxin levels
- ACE inhibitors may increase serum lithium levels
- ACE inhibitors may decrease tetracycline absorption (up to 37%) Mechanism of Action:
- drug interaction(s) of fluticasone with HIV1 protease inhibitors
- drug interaction(s) of calcineurin inhibitors with ACE inhibitors
- drug interaction(s) of calcium channel blockers with ACE inhibitors
- drug interaction(s) of renin-angiotensin-aldosterone inhibitors with trimethoprim-sulfamethoxazole
- drug interaction(s) of lithium carbonate with ACE inhibitors
- drug interaction(s) of ACE inhibitor with trimethoprim
- drug interaction(s) of ACE inhibitors with potassium-sparing diuretics
- drug interaction(s) of ACE inhibitors with aliskiren
- drug interaction(s) of ACE inhibitors with angiotensin II receptor antagonists
- drug interaction(s) of potassium chloride with ACE inhibitors
- drug interaction(s) of spironolactone with ACE inhibitors
- drug interaction(s) of diuretics with ACE inhibitors
- drug interaction(s) of beta blockers with ACE inhibitors
- drug interaction(s) of NSAIDs, diuretics & ACE inhibitors
- drug interaction(s) of NSAIDs with ACE inhibitors
- drug interaction(s) of NSAIDs & antihypertensives
More general terms
Component of
References
- ↑ The Pharmacological Basis of Therapeutics, 9th ed. Gilman et al, eds. Permagon Press/McGraw Hill, 1996.
- ↑ Geriatric Dosage Handbook, 6th edition, Selma et al eds, Lexi-Comp, Cleveland, 2001
- ↑ 3.0 3.1 Deprecated Reference
- ↑ 4.0 4.1 4.2 NEJM Knowledge+ Complex Medical Care
- ↑ 5.0 5.1 5.2 Medical Knowledge Self Assessment Program (MKSAP) 11, 16, American College of Physicians, Philadelphia 1998, 2012
Dicpinigaitis PV. Angiotensin-converting enzyme inhibitor-induced cough: ACCP evidence-based clinical practice guidelines. Chest. 2006 Jan;129(1 Suppl):169S-173S. PMID: https://www.ncbi.nlm.nih.gov/pubmed/16428706