Calcium Channel Blockers

Calcium channel blockers work by binding L-type voltage-gated calcium channels, blocking calcium influx into vascular smooth muscle cells and cardiac myocytes. Calcium entry normally triggers smooth muscle contraction and, in the heart, drives the action potential upstroke in nodal tissue and supports contractile force. By reducing calcium influx, CCBs cause vasodilation and, depending on the drug, can also slow heart rate and conduction.

Dihydropyridines

Amlodipine, nifedipine, felodipine, nicardipine, and clevidipine share the "-dipine" naming stem and act preferentially on vascular smooth muscle rather than cardiac tissue. This vascular selectivity makes them potent arterial vasodilators with little direct effect on heart rate or contractility. They lower peripheral vascular resistance, which is why they are first-line options for hypertension, particularly effective in older adults and in Black patients, populations in whom low-renin, volume- and vasoconstriction-driven hypertension responds especially well to arterial dilation. Because they relax arterial smooth muscle broadly, dihydropyridines also treat Raynaud phenomenon, where they prevent digital artery vasospasm, and vasospastic (Prinzmetal) angina, where coronary artery spasm rather than fixed atherosclerotic obstruction causes chest pain.

Non-dihydropyridines

Verapamil and diltiazem are cardioselective, acting more on the heart than the peripheral vasculature. They produce meaningful negative inotropic (reduced contractile force), negative chronotropic (slowed heart rate), and negative dromotropic (slowed AV nodal conduction) effects. These properties make them useful for rate control in supraventricular tachyarrhythmias, including atrial fibrillation and atrial flutter, where slowing AV nodal conduction reduces the ventricular response rate. They are also used for angina, since slowing heart rate and reducing contractility lowers myocardial oxygen demand.

Adverse effects and key safety points

Dihydropyridines commonly cause peripheral edema (from arteriolar dilation without matching venodilation, raising capillary hydrostatic pressure), flushing, headache, and reflex tachycardia — the heart speeding up compensatorily as blood pressure drops, since these agents do not blunt heart rate directly. Non-dihydropyridines instead risk bradycardia, AV block, and constipation (calcium channel blockade in gastrointestinal smooth muscle slows motility, especially with verapamil). Their negative inotropic effect makes verapamil and diltiazem a poor choice in heart failure with reduced ejection fraction, where further depressing contractility can worsen decompensation. Combining a non-dihydropyridine with a beta blocker is a dangerous pairing: both suppress AV conduction and contractility, risking severe bradycardia, heart block, or cardiogenic shock. Gingival hyperplasia is a class effect across dihydropyridines and non-dihydropyridines alike, requiring dental monitoring. Grapefruit juice inhibits intestinal CYP3A4, the enzyme that metabolizes most CCBs, raising drug levels and adverse-effect risk — patients should avoid it. Immediate-release nifedipine should be avoided for acute blood pressure lowering because its rapid onset can cause a precipitous drop in pressure with reflex tachycardia and has been linked to myocardial ischemia and stroke; if rapid control is needed, other agents are preferred.

Nursing considerations

Extended-release CCB tablets and capsules must be swallowed whole, never crushed, split, or chewed, since disrupting the release mechanism can cause a surge of drug and dangerous hypotension. Monitor blood pressure and heart rate before and after dosing, watch for edema and signs of heart failure with non-dihydropyridines, assess bowel patterns, and counsel on oral hygiene and avoiding grapefruit products.