Calcium antagonists

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 16.12.2020

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Ca-antagonists; Ca-Blocker; Ca channel blocker; Calcium antagonist; Calcium antagonists; Calcium blocker; Calcium blocking agent; Calcium channel blocker; calcium channel blocker, calcium channel antagonist; KA; L-channel blocker

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Calcium antagonists are substances that selectively block the voltage-dependent influx of calcium ions (Ca++) through the L-type calcium channel (L=long lasting), but do not affect other calcium channels (see below Calcium channels). Calcium antagonists reduce peripheral vascular resistance (afterload).

In the human organism, the L-type calcium channel is present in smooth muscle (e.g. in the vascular walls), in the cardiovascular system and also in neurons. In smooth muscle and cardiac muscle, the "long-lasting calcium channels", which allow a slow CalCium influx into the cell when the cell membrane is depolarized, are essential for electromechanical coupling.

Calcium antagonists are divided into 3 groups according to their chemical structure:

Phenylalkylamines and benzothiazepines (non-dihydropyrine type calcium atagonists) are also called cationic amphiphilic calcium antagonists. In contrast to dihydropiridines, they have a cardiodepressant effect even in therapeutic doses. This is due to different binding sites at the L-type calcium channel + different physical and chemical properties of the different substance groups. Calcium atagonists of the non-dihydropyrin type belong to class IV antiarrhythmics. They must not be combined with beta-blockers (risk of AV block; bradycardia).

Dihydropyrin-type calcium atagonists are vasoselective. They lower peripheral resistance. This can lead to reflex tachycardia and pectanginal symptoms. Dihydropyrin-type calcium antagonists may be combined with beta-blockers, thus avoiding reflex tachycardia.

Pharmacodynamics (Effect)
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Calcium antagonists block the calcium channel and prevent calcium from entering the cells to trigger the calcium-dependent reaction chain.

Calcium antagonists have a dilating effect on the arterial walls. The arteries remain dilated and blood pressure does not rise. The coronary vessels of the heart are also dilated. The oxygen supply to the heart is optimised.

On the heart muscles, calcium antagonists have an effect on both the strength of the contraction and the speed of the heartbeat. If the calcium channels are blocked, the heart muscles can only contract to a lesser extent. This leads to a reduction in the pumping capacity. The oxygen demand of the heart muscle is lower.

Furthermore, the conduction of excitation is slowed down. This leads to a slowing of the pulse. The excitation formation in the sinus node of the heart is also slowed down. Certain cardiac arrhythmias are improved.

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The classic indication for calcium antagonists is arterial hypertension (Wright JM et al 2018). By dilating the arteries, the vessel walls are reduced arteriosclerotic risk. The risk of thrombosis, stroke, and heart attack decreases.

The cationic amphiphilic calcium antagonists (phenylalkylamines and benzothiazepines) are additionally used in the treatment of supraventricular tachycardia.

Another indication is angina pectoris. Calcium antagonists reduce the oxygen consumption of the heart.

Pregnancy/nursing period
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Calcium antagonists have teratogenic and embryotoxic effects.

Undesirable effects
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A typical ADR of the calcium antagonists is an excessive drop in blood pressure. Often combined with flushing symptoms and headache.

Possibly oedema of the lower legs and ankles.

Cutaneous adverse reactions (see also Calcium antagonists, adverse reactions) Severe skin reactions are possible, in particular erythema exsudativum multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, AGEP (pustulosis, acute generalised exanthematous) usually occurring 7-10 days after the start of therapy and regressing 10-14 days after the end of therapy).

Other possible mucocutaneous UAWs: drug reaction, fixed; erythema, erythromelalgia, allergic skin reactions, hyperhidrosis, gingival hyperplasia, photosensitization.

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Increase of the dioxin plasma level.

Combination of verapamil/diltiazem with beta-receptor blockers is contraindicated (see above)

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Heart failure NYHA III - NYHA IV (a sharp drop in blood pressure can lead to reduced blood flow to the heart); unstable angina pectoris; acute heart attack.

Other heart diseases such as "sick sinus syndrome" or grade II and III AV block are contraindications for verapamil and diltiazem.

Verapamil can lead to constipation (can be compensated by appropriate diet)

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Amlodipine (generic drugs)

Felodipine (generic drugs)

Isradipine (Vascal®)

Leracanipine (generic drugs)

Manidipine (Maminper ®)

Nifedipine (Adalat, generic products see above)

nilvadipine (Nivadil®, Escor ®)

Nisoldipine (Baymycard ®)

Nitrendipine (generic drugs)

Verapamil (Isoptin®, generic drugs)


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  1. Gandini S et al (2018) Anti-hypertensive drugs and skin cancer risk: a review of the literature and meta-analysis.Crit Rev Oncol Hematol 122:1-9.
  2. Wright JM et al (2018) First-line drugs for hypertension. Cochrane Database Syst Rev 4:CD001841.


Last updated on: 16.12.2020