calcium channel blocker
A calcium channel blocker keeps the trigger for muscle squeezing from firing. Calcium entering a muscle cell is the spark that makes it contract; in the heart and blood vessels, that calcium flows in through tiny gated pores in the cell membrane. Block those pores and the spark is weaker, so arteries relax and the heart contracts less forcefully, easing blood pressure and cardiac strain.
These drugs block voltage-gated L-type calcium channels, but they fall into two practical groups. Dihydropyridines such as amlodipine and nifedipine act mainly on arterial smooth muscle, producing vasodilation, and are favoured for hypertension. Non-dihydropyridines, namely verapamil and diltiazem, act more on the heart itself, slowing heart rate and conduction, which makes them useful for certain arrhythmias and angina.
Side effects track the mechanism. Dihydropyridines commonly cause ankle swelling, flushing and headache from arterial dilation, and a reflex fast heartbeat. Verapamil and diltiazem can slow the heart too much and worsen heart failure, so they are generally not combined with beta-blockers, which would compound the slowing. Verapamil also frequently causes constipation.
Amlodipine, a once-daily dihydropyridine calcium channel blocker, lowers blood pressure by relaxing arteries, with mild ankle swelling as its most common complaint.
Dihydropyridines target vessels; their swelling and flushing follow directly from vasodilation.
The two subgroups behave so differently that it is safer to think of dihydropyridine vasodilators and rate-slowing verapamil/diltiazem as almost separate tools.