Calcium channel blocker

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Calcium channel blockers (CCBs) are a class of drugs and natural substances that disrupt the calcium (Ca2+) conduction of calcium channels.[1]

It has effects on many excitable cells of the body, such as cardiac muscle, i.e. heart, smooth muscles of blood vessels, or neurons. Drugs used to target neurons are used as antiepileptics and are not covered in this article.

The most widespread clinical usage of calcium channel blockers is to decrease blood pressure in patients with hypertension, with particular efficacy in treating elderly patients.[2] Also, calcium channel blockers frequently are used to control heart rate, prevent cerebral vasospasm, and reduce chest pain due to angina pectoris.


Most calcium channel blockers decrease the force of contraction of the myocardium (muscle of the heart). This is known as the negative inotropic effect of calcium channel blockers. It is because of the negative inotropic effects of most calcium channel blockers that they are avoided (or used with caution) in individuals with cardiomyopathy.

Many calcium channel blockers also slow down the conduction of electrical activity within the heart, by blocking the calcium channel during the plateau phase of the action potential of the heart (see: cardiac action potential). This results in a negative chronotropic effect resulting in a lowering of the heart rate and the potential for heart block. The negative chronotropic effects of calcium channel blockers make them a commonly used class of agents in individuals with atrial fibrillation or flutter in whom control of the heart rate is an issue. Negative chronotropy can be beneficial in that elevated heart rate can result in significantly higher 'cardiac work', which can result in anginal symptoms: lower heart rates represent lower cardiac oxygen requirements.

Pharmacologic Beta blockade is superior to Calcium channel blockade regarding chronotropic properties of the myocardium. Titration of a Beta Blocker to a desired heart rate is decidedly easier than titration of a non dihydropyridine CCB.

Mechanism of action

Calcium channel blockers work by blocking voltage-gated calcium channels (VGCCs) in cardiac muscle and blood vessels. This decreases intracellular calcium leading to a reduction in muscle contraction. In the heart, a decrease in calcium available for each beat results in a decrease in cardiac contractility. In blood vessels, a decrease in calcium results in less contraction of the vascular smooth muscle and therefore an increase in arterial diameter (CCB's do not work on venous smooth muscle), a phenomenon called vasodilation. Vasodilation decreases total peripheral resistance, while a decrease in cardiac contractility decreases cardiac output. Since blood pressure is determined by cardiac output and peripheral resistance, blood pressure drops. Calcium channel blockers are especially effective against large vessel stiffness, one of the common causes of elevated systolic blood pressure in elderly patients.[2]

With a relatively low blood pressure, the afterload on the heart decreases; this decreases the amount of oxygen required by the heart. This can help ameliorate symptoms of ischemic heart disease such as angina pectoris.

Unlike β-blockers, calcium channel blockers do not decrease the responsiveness of the heart to input from the sympathetic nervous system. Since moment-to-moment blood pressure regulation is carried out by the sympathetic nervous system (via the baroreceptor reflex), calcium channel blockers allow blood pressure to be maintained more effectively than do β-blockers.

However, because calcium channel blockers result in a decrease in blood pressure, the baroreceptor reflex often initiates a reflexive increase in sympathetic activity leading to increased heart rate and contractility. A β-blocker may be combined with a dihydropyridine calcium channel blocker to minimize these effects.

Ionic calcium is antagonized by magnesium ions in the nervous system. Because of this, dietary supplements of magnesium oxide and other magnesium preparations may increase or enhance the effects of calcium channel blockade.[3]

Classes of calcium channel blockers


Dihydropyridine calcium channel blockers are often used to reduce systemic vascular resistance and arterial pressure, but are not used to treat angina (with the exception of amlodipine, nicardipine, and nifedipine, which carry an indication to treat chronic stable angina as well as vasospastic angina) because the vasodilation and hypotension can lead to reflex tachycardia. Dyhydropiridine calcium chanel blockers can worsen proteinuria in patients with nephropathy.[4] This CCB class is easily identified by the suffix "-dipine".

Side effects of these synthetic drugs may include but are not limited to:

  • Dizziness, headache, redness in the face
  • Fluid buildup in the legs
  • Rapid heart rate.
  • Slow heart rate.
  • Constipation
  • Gingival overgrowth



Phenylalkylamine calcium channel blockers are relatively selective for myocardium, reduce myocardial oxygen demand and reverse coronary vasospasm, and are often used to treat angina. They have minimal vasodilatory effects compared with dihydropyridines and therefore cause less reflex tachycardia, making it appealing for treatment of angina, where tachycardia can be the most significant contributor to the heart's need for oxygen. Therefore, as vasodilation is minimal with the phenylalkylamines, the major mechanism of action is causing negative inotropy. Phenylalkylamines are thought to access calcium channels from the intracellular side, although the evidence is somewhat mixed [5].


Benzothiazepine calcium channel blockers are an intermediate class between phenylalkylamine and dihydropyridines in their selectivity for vascular calcium channels. By having both cardiac depressant and vasodilator actions, benzothiazepines are able to reduce arterial pressure without producing the same degree of reflex cardiac stimulation caused by dihydropyridines.


While most of the agents listed above are relatively selective, there are additional agents that are considered nonselective. These include mibefradil, bepridil and fluspirilene.[6]

Another example is fendiline.[7]

Other drugs with similar uses

Other classes of pharmaceutical agents that have overlapping effects as calcium channel blockers include ACE inhibitors, beta-blockers, and nitrates.


Mild CCB toxicity is treated with supportive care. Non-dihydropyridine CCB may produce profound toxicity and early decontamination, especially for slow release agents, is essential. Treatment involves intravenous calcium, atropine, fluids, insulin and inotropes. Insulin is required because at high doses CCB block the effect of insulin. If unsuccessful ventricular pacing should be used.[8]

See also


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External links

ar:محصرات قنوات الكالسيوم

ca:Blocador dels canals de calci de:Calciumantagonist es:Bloqueador de canales de calcio fa:بلوک‌کننده کانال کلسیم fr:Bloqueurs de canaux calciques it:Calcio-antagonisti nl:Calciumantagonist ja:カルシウム拮抗剤 pl:Antagoniści kanału wapniowego pt:Bloqueador dos canais de cálcio ru:Антагонисты кальция sv:Kalciumhämmare

  1. calcium channel blocker at Dorland's Medical Dictionary
  2. 2.0 2.1 Nelson, Mark. "Drug treatment of elevated blood pressure". Australian Prescriber (33): 108–112. Retrieved August 11 2010.  Check date values in: |access-date= (help)
  3. 1. Iseri LT & French JH. “Magnesium: nature’s physiologic calcium blocker.” Am Heart J, 108, 188-193, 1984.
  4. Remuzzi G, Scheppati A, Ruggenenti P: Nephropathy in patients with type 2 diabetes. N Engl J Med 2002;346:1145.
  5. Hockerman et al, Annu Rev Pharmacol Toxicol. 1997;37:361-96
  6. Lua error in package.lua at line 80: module 'Module:Citation/CS1/Suggestions' not found.
  7. Scultéty S, Tamáskovits E (1991). "Effect of Ca2+ antagonists on isolated rabbit detrusor muscle". Acta Physiol Hung. 77 (3-4): 269–78. PMID 1755331. 
  8. Calcium Channel Blockers. Medicine 2007;35:599-602