Learning Objective:

By the end of this section, learners will be able to describe the mechanism of action of calcium-channel blockers, differentiate their cardiac versus vascular effects, and predict their clinical uses and adverse effects in cardiovascular disease.

Calcium-channel blockers (CCBs) inhibit L-type Ca²⁺ channels in cardiac myocytes and vascular smooth muscle.

This leads to:

• ↓ intracellular Ca²⁺
• ↓ cardiac contractility and heart rate → ↓ cardiac output (primarily verapamil and diltiazem)
• ↓ vascular smooth muscle tone → ↓ total peripheral resistance (all CCBs)

Drug classes:

• Non-dihydropyridines: verapamil, diltiazem (greater cardiac effects)
• Dihydropyridines: “-dipines” (e.g., nifedipine; greater vascular selectivity)

Physiologic effects:

• Verapamil and diltiazem → ↓ HR, ↓ AV conduction, ↓ CO
• Dihydropyridines → potent arteriolar vasodilation → ↓ TPR

Clinical Uses

• Hypertension – all CCBs
• Angina pectoris – all CCBs
• Arrhythmias (rate control) – verapamil, diltiazem

Adverse Effects

• Reflex tachycardia – dihydropyridines
• Gingival hyperplasia – dihydropyridines
• Constipation – verapamil

Clinical Correlate

Beta blockers are not first-line agents for uncomplicated hypertension, but they are preferred in patients with specific comorbidities such as stable angina, chronic heart failure, or prior myocardial infarction, where their additional cardioprotective effects are beneficial.

Activity