Category:Calcium-channel Blocker, CCB: Difference between revisions

Calcium-channel blockers Calcium-channel blockers are used mainly in the management of angina, hypertension, and cardiac arrhythmias. Calcium-channel blockers inhibit the cellular influx of calcium that is responsible for maintenance of the plateau phase of the action potential. Thus calcium-channel blockers mainly affect tissues in which depolarization is dependent upon calcium rather than sodium influx, such as vascular smooth muscle, myocardial cells, and cells within the sino-atrial (SA) and atrioventricular (AV) nodes.

The main actions of the calcium-channel blockers include:

• dilatation of coronary and peripheral arteries and arterioles with little or no effect on venous tone,
• a negative inotropic action,
• reduction of heart rate, and
• slowing of AV conduction.

However, the effects of individual drugs, and therefore their uses, are modified by their selectivity of action at different tissue sites. Traditionally, calcium-channel blockers have been classified according to their chemical structure; other methods of classification relate to the subtypes of calcium channels which they block, and their effects on heart rate. There are three major groups that are highly specific blockers of calcium channels.

Dihydropyridine calcium-channel blockers (such as amlodipine) act on slow, L-type (long) channels. They have a greater selectivity for vascular smooth muscle than for myocardium and therefore their main effect is vasodilatation. They are non-rate-limiting, with little or no action at the SA or AV nodes, and negative inotropic activity is rarely seen at therapeutic doses. They are used for their antihypertensive and anti-anginal properties.

Benzothiazepine calcium-channel blockers (such as diltiazem) and phenylalkylamine calcium-channel blockers (such as verapamil) also act on L-type channels, but they have less selective vasodilator activity than dihydropyridine derivatives. They are classed as rate-limiting and have a direct effect on myocardium, causing depression of SA and AV nodal conduction. They are used for supraventricular arrhythmias as well as angina and hypertension.