Calcium channel blockers

Last updated: September 6, 2023

Summarytoggle arrow icon

Calcium channel blockers (CCBs) are drugs that bind to and block L-type calcium channels, which are the predominant calcium channels in the myocardium and vascular smooth muscles. By blocking these channels, CCBs cause peripheral arterial vasodilation (leading to a drop in blood pressure) and myocardial depression (leading to negative chronotropic, inotropic, and dromotropic effects on the myocardium). CCBs are classified into two major groups according to the main site of action: Dihydropyridines (e.g., nifedipine, amlodipine) are potent vasodilators, and nondihydropyridines (e.g., verapamil) are potent myocardial depressants. Diltiazem, a common nondihydropyridine, has moderate vasodilatory and myocardial depressant effects. Nondihydropyridines are also categorized as class IV antiarrhythmic drugs and are used in the treatment of supraventricular arrhythmias. The most common indications for CCB use are arterial hypertension and stable angina. The main side effects of dihydropyridines are caused by vasodilation (e.g., headache, peripheral edema); those of nondihydropyridines are caused by myocardial depression (e.g., bradyarrhythmias, atrioventricular block). CCBs are contraindicated in patients with preexisting cardiac conduction disorders, symptomatic hypotension, and/or acute coronary syndrome.

See also “Calcium channel blocker poisoning.”

Overviewtoggle arrow icon

Overview of calcium channel blockers [1]
Agents Effects Side effects Indications
Dihydropyridines [2][3]
  • Short-acting : nifedipine, clevidipine, nimodipine
  • Intermediate-acting : nitrendipine, nicardipine, lercanidipine
  • Long-acting : amlodipine, felodipine
  • Benzothiazepines: diltiazem
  • Phenylalkylamines: verapamil, gallopamil

Pharmacodynamicstoggle arrow icon

Dihydropyridine CCBs (nifedipine and amlodipine) primarily act on vascular smooth muscles. Nondihydropyridine CCBs (verapamil > diltiazem) primarily act on the heart.

Verapamil mainly acts on Ventricles and Amlodipine mainly acts on Arteries.

Indicationstoggle arrow icon

All CCBs [4]



Short-acting CCBs (e.g., nifedipine) are not indicated for monotherapy of angina because they cause hypotension and secondary reflex tachycardia, which can worsen cardiac ischemia.

Adverse effectstoggle arrow icon

Dihydropyridines [5][6]

Due to their vasodilatory effects, dihydropyridines should be considered in the differential diagnosis of peripheral edema.

Nondihydropyridines [6]

We list the most important adverse effects. The selection is not exhaustive.

Contraindicationstoggle arrow icon

All CCBs [10]


Nondihydropyridines [16]

Nondihydropyridine CCBs should not be combined with beta blockers because CCBs can enhance the negative inotropic, chronotropic, and dromotropic effects of beta blockers.

Phenylalkylamines (e.g., verapamil), which primarily affect the calcium channels of the heart, are contraindicated in cases of heart failure because of their negative effect on myocardial contractility.

We list the most important contraindications. The selection is not exhaustive.

Referencestoggle arrow icon

  1. Katzung B,Trevor A. Basic and Clinical Pharmacology. McGraw-Hill Education ; 2014
  2. Nicardipine. Updated: January 20, 2016. Accessed: November 23, 2017.
  3. Clevidipine. Updated: October 6, 2017. Accessed: November 23, 2017.
  4. Sica DA. Calcium channel blocker-related periperal edema: can it be resolved?. J Clin Hypertens. 2003; 5 (4): p.291–295.doi: 10.1111/j.1524-6175.2003.02402.x . | Open in Read by QxMD
  5. Basile J. The Role of Existing and Newer Calcium Channel Blockers in the Treatment of Hypertension. J Clin Hypertens. 2004; 6 (11): p.621-629.doi: 10.1111/j.1524-6175.2004.03683.x . | Open in Read by QxMD
  6. Ozawa Y, Hayashi K, Kobori H. New Generation Calcium Channel Blockers in Hypertensive Treatment. Curr Hypertens Rev. 2006; 2 (2): p.103-111.doi: 10.2174/157340206776877370 . | Open in Read by QxMD
  7. Calcium Channel Blockers (CCBs). Updated: December 1, 2008. Accessed: April 6, 2017.
  8. Kelley SR, Kamal TJ, Molitch ME. Mechanism of verapamil calcium channel blockade-induced hyperprolactinemia.. Am J Physiol. 1996; 270 (1 Pt 1): p.E96-100.doi: 10.1152/ajpendo.1996.270.1.E96 . | Open in Read by QxMD
  9. Nifedipine. Updated: March 13, 2019. Accessed: September 23, 2019.
  10. Collard CL. Hypertension: Medication update. South Med J. 2001; 94 (11): p.1065-1070.
  11. Nifedipine Disease Interactions. Updated: April 6, 2017. Accessed: April 6, 2017.
  12. Held PH, Yusuf S, Furberg CD. Calcium channel blockers in acute myocardial infarction and unstable angina: an overview. BMJ. 1989; 299: p.1187.doi: 10.1136/bmj.299.6709.1187 . | Open in Read by QxMD
  13. Marian AJ. Contemporary treatment of hypertrophic cardiomyopathy. Tex Heart Inst J. 2009; 36 (3): p.194-204.
  14. Opie LH. Calcium channel antagonists part IV: Side effects and contraindications drug interactions and combinations. Cardiovasc Drugs Ther. 1988; 2 (2): p.177–189.doi: 10.1007/BF00051233 . | Open in Read by QxMD
  15. Rossi S. Australian Medicines Handbook 2014. Australian Medicines Handbook ; 2014
  16. Calcium-Channel Blockers (CCBs). Updated: March 22, 2015. Accessed: April 6, 2017.
  17. Pre-excitation Syndromes. Updated: May 31, 2016. Accessed: February 13, 2017.
  18. Kusumoto FM, Schoenfeld MH, Barrett C, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay. J Am Coll Cardiol. 2019; 74 (7): p.e51-e156.doi: 10.1016/j.jacc.2018.10.044 . | Open in Read by QxMD
  19. St-Onge M, Anseeuw K, et al. Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults. Crit Care Med. 2017; 45 (3): p.e306-e315.doi: 10.1097/ccm.0000000000002087 . | Open in Read by QxMD
  20. Chakraborty RK, Hamilton RJ. Calcium Channel Blocker Toxicity. StatPearls. 2019.

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