Atenolol
Atenolol
Generic Name
Atenolol
Mechanism
Atenolol competitively antagonizes β₁‑adrenergic receptors in the myocardium, resulting in:
• ↓ Sympathetic stimulation → Reduced heart rate (negative chronotropy)
• ↓ Myocardial contractility (negative inotropy)
• ↓ Renal renin release → Lower angiotensin‑II formation
• ↓ Sympathetic‑mediated vasoconstriction → Decreased cardiac output and systemic blood pressure
The net effect is a decrease in myocardial oxygen demand and improvement in coronary perfusion.
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Pharmacokinetics
| Parameter | Data |
| Absorption | Oral bioavailability ≈ 50 % (dose‑dependent). Peak plasma concentration (Tmax) 1–4 h. |
| Distribution | Low lipophilicity → minimal CNS penetration; volume of distribution (Vd) ≈ 1.0–1.3 L/kg. |
| Metabolism | Minimal first‑pass hepatic metabolism; ~20 % undergoes glucuronidation/oxidative conjugation. |
| Elimination | Mainly renal (≈ 80 % unchanged). Half‑life ≈ 6–7 h (up to 15 h in renal impairment). |
| Renal excretion | Creatinine clearance < 60 mL/min → dose adjustment required. |
| Drug interactions | Concomitant CYP2D6 substrates may affect β‑blocker pharmacodynamics; modest potential with CYP2D6 inducers (e.g., rifampin). |
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Indications
- Hypertension – first‑line in patients requiring a cardio‑selective β‑blocker.
- Stable angina pectoris – reduces angina frequency and improves exercise tolerance.
- Post‑myocardial infarction (MI) – ↓re‑infarction risk and improve survival.
- Vasovagal syncope – prevention of recurrent episodes.
- Supraventricular tachycardia (SVT) – as an adjunctive rhythm‑control agent.
- Hyperthyroidism‑related tachycardia – controls cardiac manifestations.
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Contraindications
- Absolute:
- Severe bradycardia, second‑ or third‑degree atrioventricular block (unless pacer).
- Systolic heart failure with reduced ejection fraction (in most β‑blocker‑sensitive patients).
- Known hypersensitivity to atenolol or other β‑blockers.
- Relative:
- Asthma/COPD – caution due to β₂ blockade at high doses.
- Diabetic patients – mask hypoglycemia symptoms.
- Peripheral arterial disease – may worsen ischaemia.
- Severe hepatic impairment – limited data.
- Warnings:
- Non‑reversible pulmonary disease → avoid or use with extreme caution.
- Congestive heart failure in early stages – monitor for decompensation.
- Uncontrolled arrhythmias – may precipitate conduction arrest.
- Renal impairment – requires dose adjustment.
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Dosing
| Condition | Starting Dose (oral) | Titration | Max Dose |
| Hypertension | 50 mg once daily | Increase by 50 mg/d to a maximum of 200 mg | 200 mg/d |
| Angina (stable) | 50 mg daily | Increase by 50 mg/d as tolerated, up to 200 mg | 200 mg/d |
| Post‑MI | 25 mg twice daily | Continue 50–100 mg BID | 200 mg/d |
| SVT | 50 mg BID | Adjust per ECG | 200 mg/d |
| Vasovagal syncope | 50 mg twice daily | Incrementally to 200 mg/d | 200 mg/d |
• Administration: Take with food to reduce GI irritation.
• Renal adjustment: CrCl 30–60 mL/min → decrease dose by 25 %; CrCl < 30 mL/min → avoid.
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Adverse Effects
| Category | Examples | Notes |
| Cardiovascular | Bradycardia, fatigue, dizziness, hypotension | Monitor pulse/ BP, especially in elderly |
| Respiratory | Mild bronchoconstriction | Use cautiously in asthmatics |
| Metabolic | Masked hypoglycemia symptoms, mild hyperglycemia | Check glucose in diabetics |
| Dermatologic | Rash, pruritus | Rare; treat with antihistamines |
| Central nervous | Anosmia, headache, insomnia (rare due to low lipophilicity) | Generally minimal |
| Serious | Severe bradyarrhythmias, heart failure decompensation, exacerbated COPD | Immediate medical attention |
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Monitoring
- Baseline: ECG, BP, HR, cardiac output (if available), renal function.
- During therapy:
- Blood pressure & heart rate ≥ weekly until stable.
- Post‑MI patients: ECG 24 h post‑dose; monitor QTc.
- Diabetic subjects: blood glucose 2–3 ×/day.
- Renal function every 4–6 weeks in chronic kidney disease (CKD).
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Clinical Pearls
- Low‑lipophilicity = CNS safety – favor atenolol when a β₁‑selective agent is desired with minimal central nervous side‑effects (e.g., insomnia, depression).
- Glucuronidation → Minimal drug–drug interactions with many CYP450 substrates; safe in polypharmacy settings.
- Renal dosing: Because 80 % is renally excreted, accurate creatinine clearance estimation is essential; consider switching to a non‑renal agent (e.g., bisoprolol) if CrCl 20 % reduction per month is a good compliance indicator; > 30 % may signal need to reduce dose.
- Asthma/COPD caution: Start at ≤ 50 mg/d and titrate slowly; consider pre‑medication with inhaled β₂‑agonist if clinically indicated.
Remember: Atenolol’s pharmacologic profile (selective β₁ blockade, renal elimination, minimal CYP involvement) makes it an excellent first‑line β‑blocker in patients where central side‑effects, hepatic metabolism, or drug interactions pose significant concerns.