Calcium Channel Blockers



  • Drugs blocking L-type of voltage-gated calcium channels, present in blood vessels & heart.

Drug groups:

  • Three groups of drugs:
  • Phenylalkylamines – 
    • Verapamil, nor-verapamil.
  • Benzothiazepines – 
    • Diltiazem.
  • Dihydropyridines – 
    • Nifedipine, nicardipine, nimodipine, nisoldipine, nitrendipine, isradipine, lacidipine, felodipine & amlodipine.

Drug actions of CCB’s:

  • Inhibits calcium channels & reduces frequency of Ca+ channels opening –> Results in vasodilation.
  • Smooth muscle relaxation in blood vessels & extravascular organs (bronchus, GIT, urinary bladder, uterus).

CCB’s & cardiac activity:

  • Decreased cardiac activity – 
    • Decreased heart rate, AV conduction & contractility.
  • Little direct cardiac activity:
    • Dihydropyridine (DHP) group.
    • Acts mainly on blood vessels – Hence, called peripherally acting CCBs.
  • Strong direct cardiac activity:
    • Verapamil & diltiazem (verapamil > diltiazem).
    • Strong cardiodepressant activity.

Effect of different CCBs on HR & BP:


Blood vessel


Heart rate

Direct action

Reflex action

Net action

Verapamil Vasodilation Decreases BP Strong reduction Increases HR Mild reduction
Diltiazem Vasodilation Decreases BP Mild reduction Increases HR Little reduction
DHP Vasodilation Decreases BP No effect Increases HR Increases HR

General indications of CCB’s:

  • Used in angina (both classical & variant angina)
    • Mainly Verapamil, diltiazem & long acting DHPs.
  • DOC for hypertensive patients with migraine.
    • Eg: Flunarizine (weak CCB) – For prophylaxis of migraine.
  • In hypertensive patients with PVD (peripheral vascular diseases – Raynaud’s phenomena).

General contraindications of CCB’s:

  • In sick sinus syndrome –
    • Because of CCB’s reflex tachycardia.
  • In angina –
    • Precipitates acute attack of angina
    • Accentuates angina symptoms by causing tachycardia (Except short-acting DHPs like nifedipine).
  • In Hyperglycemia (mainly Nifedipine):
    • By decreasing insulin release.
  • CCB’s along with β-blockers.

General adverse effects of CCB’s:

  • Reflex tachycardia:
    • Caused due to vasodilatory action.
    • Mainly by DHP’s drugs.
    • Nifedipine (short half-life) – More marked tachycardia.
    • Amlodipine – Long-acting drugs (maximum half-life) – Less tachycardia.
    • This effect nullified by direct cardiodepressant action (except DHPs).
  • Voiding difficulty in elderly:
    • Due to urinary bladder relaxation.
  • Constipation & ankle edema (particularly verapamil).
  • Increases plasma digoxin concentration –
    • By decreasing its excretion.

Individual drug description:

1. Verapamil:

  • Actions:
    • Maximum cardio-depressant action.
    • Causes vasodilation – By blocking calcium channel.
    • Maximum effect on cardiac conduction.
    • Increases PR interval.
  • Metabolic properties:
    • Maximum plasma protein-bound drug.
    • CYP3A inhibitor.
    • Has racemic mixture of two enantiomers with different pharmacokinetic & pharmacodynamic properties.
  • Indications:
    • Treatment of angina, PSVT, hypertension & hypertrophic obstructive cardiomyopathy (HOCM).

2. Diltiazem:

  • Lesser effect on heart than verapamil.
  • Uses:
    • Same indication as verapamil.
    • Suitable for elderly patients, low renin hypertension cases, asthma, migraine or peripheral vascular disease & isolated systolic hypertensive cases.

3. Dihydropyridine drug group:

  • Safe in pregnancy.

3a.) Nifedipine:

  • Predominant peripheral action.
  • Increases angina risk.
    • Increases heart rate & thus cardiac work.
    • Prevented by sustained-release preparation of nifedipine & amlodipine.
  • Possesses natriuretic property.
  • Interferes with anesthesia.
  • Nifedipine & beta-blocker given together – To overcome nifedipine’s increased sympathetic activity.
  • History:
    • Previously used sublingually for hypertensive emergencies.
    • Banned due to increased risk of MI & mortality.
  • Uses:
    • For Achalasia cardia.

3b.) Nicardipine:

  • Longest acting parenteral CCB.
  • DOC for hypertensive emergencies.
  • Combined with beta blockers to avoid tachycardia.

3c.) Nimodipine:

  • Shortest acting CCB’s
  • Relatively Cerebro-selective vasodilator.
  • Used for reversal of compensatory vasoconstriction after subarachnoid hemorrhage.

3d.) Clevidipine:

  • Ultrashort-acting DHP.
  • Recently approved for hypertensive emergencies.
3e.) Amlodipine:
  • DOC for managing asthmatic patient with hypertension.
  • Rebound hypertension is seen.

Exam Important


  • Calcium channel blockers block L-type of voltage-gated calcium channels present in blood vessels & heart. 
  • CCB’s causes vasodilation by inhibits calcium channels & reduces frequency of Ca+ channels opening.
  • CCB’s reduces cardiac activity including heart rate, AV conduction & contractility.
  • Dihydropyridine (DHP) group of CCB drugs are referred to as peripherally acting CCB’s.
  • Strong cardio-depressant activity is mainly exhibited by verapamil & diltiazem (verapamil > diltiazem).
  • CCB’s are indicated for both classical & variant angina, mainly verapamil, diltiazem & long acting DHPs.
  • DOC for hypertensive patients with migraine is calcium channel blocker.
  • Flunarizine is weak CCB used for prophylaxis of migraine.
  • CCB’s are used in hypertensive patients with PVD (Raynaud’s phenomena).
  • CCB’s are contraindicated in sick sinus syndrome, as it causes reflex tachycardia.
  • Short-acting DHPs like nifedipine accentuates angina symptoms, by causing tachycardia & precipitates acute anginal attack.
  • Nifedipine causes hyperglycemia by decreasing insulin release.
  • CCB’s along with β-blockers are contraindicated.
  • Nifedipine shows marked tachycardia.
  • Long-acting CCB’s like Amlodipine will show less tachycardiac effects.
  • CCB’s causes urinary bladder relaxation, resulting in voiding difficulty in elderly.
  • CCB’s increases plasma digoxin concentration, by decreasing its excretion.
  • Verapamil shows maximum cardio-depressant action.
  • Verapamil exhibits maximum effect on cardiac conduction.
  • Verapamil increases PR interval.
  • CCB with maximum plasma protein-bound nature is verapamil.
  • Verapamil has racemic mixture of two enantiomers with different pharmacokinetic & pharmacodynamic properties.
  • Verapamil is used for treatment of angina, PSVT, hypertension & hypertrophic obstructive cardiomyopathy (HOCM).
  • Among CCB’s, dihydropyridine drugs are safer in pregnancy.
  • Nifedipine has predominant peripheral action.
  • Nifedipine by increases angina risk by increasing heart rate & thus cardiac work.
  • Nifedipine interferes with anesthesia.
  • Mostly Nifedipine & beta-blocker are given together, to overcome nifedipine’s increased sympathetic activity.
  • Nifedipine is banned for sublingual usage for hypertensive emergencies, due to increased risk of MI & mortality.
  • Nifedipine is also used for achalasia cardia.
  • Longest acting parenteral CCB is Nicardipine.
  • DOC for hypertensive emergencies is Nicardipine.
  • Nimodipine is shortest acting CCB’s with relatively cerebro-selective vasodilating nature.
  • Nimodipine is used for reversal of compensatory vasoconstriction after subarachnoid hemorrhage.
  • Clevidipine is an ultrashort-acting DHP.
  • Clevidipine is recently approved for hypertensive emergencies.
  • Amlodipine is DOC for managing asthmatic patient with hypertension.
  • Rebound hypertension is seen with Amlodipine.


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