Amlodipine Classification
Amlodipine is a dihydropyridine calcium channel blocker that selectively inhibits L-type calcium channels in vascular smooth muscle, producing peripheral arterial vasodilation with minimal effects on cardiac contractility or conduction. 1, 2
Structural and Pharmacological Classification
Amlodipine belongs to the dihydropyridine subclass of calcium channel blockers, distinguishing it from non-dihydropyridine agents (diltiazem and verapamil) 1, 2
The drug inhibits calcium influx through high-voltage-activated L-type calcium channels located in arterial smooth muscle and myocardium 1
Dihydropyridines like amlodipine demonstrate high selectivity for vascular L-type channels over myocardial channels, resulting in pronounced vasodilation without significant negative inotropic or chronotropic effects 1, 3
Mechanism Distinguishing Dihydropyridines from Non-Dihydropyridines
Unlike non-dihydropyridine calcium channel blockers (diltiazem, verapamil), amlodipine has minimal effects on cardiac conduction, atrioventricular node function, and sinus node function 3
Non-dihydropyridines are less selective for vasculature and produce more pronounced negative inotropic and chronotropic effects through actions on myocardial contractility and cardiac pacemaker cells 1
This selectivity profile makes amlodipine safer in certain cardiac conditions where preservation of cardiac conduction is critical 3
Pharmacokinetic Characteristics
Amlodipine is a long-acting dihydropyridine with an elimination half-life of 35-50 hours, allowing once-daily dosing with sustained 24-hour blood pressure control 2, 4
The drug exhibits slow absorption (peak plasma concentration at 6-8 hours) and gradual onset of effect, minimizing reflex tachycardia commonly seen with short-acting dihydropyridines 1, 2
Amlodipine is metabolized by cytochrome P450 3A4 in the liver 1
Clinical Classification Context
Amlodipine is FDA-approved for hypertension, chronic stable angina, and vasospastic angina 2
Among dihydropyridines, amlodipine (along with felodipine) has been studied specifically in heart failure populations and demonstrated neutral effects on mortality, unlike non-dihydropyridines which are contraindicated in heart failure with reduced ejection fraction 1
Rapid-release, short-acting dihydropyridines must be avoided without concomitant beta-blockade due to increased adverse potential from reflex tachycardia, though this concern does not apply to long-acting amlodipine 3