calcium channel blocker
Summary
Calcium channel blockers (CCBs) are antihypertensive/antianginal drugs that block L-type voltage-gated calcium channels in vascular smooth muscle and cardiac tissue, causing vasodilation and reduced cardiac contractility/conduction. They are divided into dihydropyridines (e.g., amlodipine, nifedipine) which are more vascular-selective, and non-dihydropyridines (verapamil, diltiazem) which have greater cardiac effects.
Detail
CCBs inhibit calcium influx through L-type calcium channels, decreasing intracellular calcium in vascular smooth muscle and cardiac myocytes. This leads to smooth muscle relaxation (vasodilation) and, in cardiac tissue, decreased contractility (negative inotropy), decreased heart rate (negative chronotropy), and slowed AV nodal conduction (negative dromotropy).
Dihydropyridines (amlodipine, nifedipine, nicardipine) preferentially act on vascular smooth muscle, causing potent peripheral vasodilation with minimal cardiac depression; reflex tachycardia can occur. Used for hypertension, chronic stable angina, and Raynaud phenomenon. Side effects include peripheral edema, flushing, headache, and gingival hyperplasia.
Non-dihydropyridines (verapamil > diltiazem) have more pronounced cardiac effects, slowing AV conduction and reducing heart rate, making them useful for supraventricular tachyarrhythmias (e.g., rate control in atrial fibrillation) and Prinzmetal angina. Verapamil has the greatest negative inotropic effect and can cause constipation; diltiazem is intermediate between verapamil and dihydropyridines.
Clinical uses: hypertension, angina (including vasospastic/Prinzmetal), Raynaud phenomenon, migraine prophylaxis, and arrhythmias (non-DHP only). Contraindicated or used cautiously in heart failure with reduced EF (especially verapamil/diltiazem) and in combination with beta-blockers (risk of severe bradycardia/AV block, especially with verapamil).
Toxicity: CCB overdose causes hypotension, bradycardia, and cardiogenic shock; treatment includes IV calcium, glucagon, insulin-dextrose (hyperinsulinemia-euglycemia therapy), and vasopressors.
Mechanistically important for boards: L-type calcium channels are found in cardiac and smooth muscle; blocking them decreases calcium-induced calcium release from the sarcoplasmic reticulum, reducing the strength of contraction and slowing SA/AV nodal depolarization.
Sources
- Katzung's Basic and Clinical Pharmacology
- First Aid for the USMLE Step 1
- Goodman & Gilman's The Pharmacological Basis of Therapeutics
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