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  • International: Adalat
  • Palestine: Angilat




Calcium channel blockers act on myocardial cells and on vascular smooth muscle (coronary artery vascular smooth-muscle and peripheral arteries vascular smooth-muscle); For a normal functioning of these cells, the intracellular calcium concentration must be increased. This usually takes place through the flow of extracellular calcium ions into the cell through the calcium channels located in the cell membrane and through the release of calcium from the sarcoplasmic reticulum. This way, calcium plays an important role in the maintenance of vascular tone and in cardiac conduction and contractility.

Calcium channel blockers block movement of extracellular calcium into cells through voltage-gated channels, thus inhibiting the activation of the actin-myosin complex and muscular contraction. Coronary artery and peripheral arteries dilate and myocardial contractility and conduction velocity decrease.

There are three different classes of calcium channel blockers. One of these classes are the dihydropyridine derivatives, characterized by a marked vasoselectivity and poor cardiac effects.

Nifedipine is a dihydropyridine calcium channel blocker. It dilates peripheral and coronary arteries without having significant action on the heart rate. (non-dihydropyridine calcium channel blockers can slow down the heart rate)

The reduction in peripheral vascular resistance leads to a reduction of blood pressure and myocardial oxygen consumption by reducing afterload. Coronary arteries dilation increases the blood flow and myocardial oxygen delivery resulting in a reduction of angina attacks.


  • Treatment of mild to moderate hypertension
  • Prophylaxis of chronic stable angina pectoris
  • Migraine prophylaxis (Off-label)
  • Preterm labor, to slow uterine contractions (Off-label) [1]
  • Raynaud's syndrome (Off-label)

[edit] DOSAGE

The treatment should be tailored to the needs of the individual patient, according to the severity of the disease and the patient's response.

Adults The recommended dosage is 20 mg twice daily swallowed with a little water during or after food, with subsequent titration of dosage according to response. The dosage may be adjusted within the range of 10-40 mg twice daily.

The recommended interval between individual doses is about 12 hours and should not be less than 4 hours.

Patients with hepatic dysfunction should commence therapy at 10 mg twice daily with careful monitoring. Patients with renal impairment do not require adjustment of dosage; treatment may be continued indefinitely.


  • Known hypersensitivity to Nifedipine.
  • Pregnancy and breastfeeding
  • Cases of cardiovascular shock.


Excessive hypotension
The hypotensive effect of Nifedipine in most patients is modest and well tolerated; however, occasional patients have had excessive and poorly tolerated hypotension during initial titration or at a time of subsequent upward dosage adjustment. This has mostly occurred in patients on concomitant Beta blocker therapy.

Beta blockers withdrawal
Patients recently withdrawn from Beta blockers may develop a withdrawal syndrome with increased angina, probably related to increased sensitivity to catecholamines. Initiation of Nifedipine treatment will not prevent this occurrence and might be expected to exacerbate it by provoking reflex catecholamine release. There have been occasional reports of increased angina in a setting of Beta blocker withdrawal and Nifedipine initiation. If possible, it is important to gradually withdraw the Beta blocker therapy, rather than stopping it abruptly, before commencing Nifedipine.

Congestive heart failure
Patients usually receiving a Beta blocker have rarely developed heart failure after beginning with Nifedipine. Patients with tight aortic stenosis may be at greater risk for such an event, as the unloading effect of Nifedipine would be expected to be of less benefit to these patients, owing to their fixed impedance to flow across the aortic valve.


  • Azole antifungals (ketoconazole, itraconazole or fluconazole): may result in increased exposure to nifedipine when co-administered.
  • Carbamazepine: reduce the bioavailability and efficacy of nifedipine
  • Diltiazem: Caution should be exercised when co-administering diltiazem and nifedipine and a reduction of the dose of nifedipine should be considered.
  • Verapamil: can inhibit the metabolism of nifedipine and increase the exposure to nifedipine during concomitant therapy. Blood pressure should be monitored and reduction of the dose of nifedipine considered.
  • Digoxin: The simultaneous administration of nifedipine and digoxin may lead to reduced clearance resulting in an increase in plasma concentrations of digoxin. Since there have been isolated reports of patients with elevated digoxin levels, and there is a possible interaction between digoxin and Nifedipine, it is recommended that digoxin levels be monitored when initiating, adjusting and discontinuing Nifedipine to avoid possible over- or under- digitalization.
  • Erythromycin, Clarithromycin: may result in increased exposure to nifedipine when co-administered.
  • Fluoxetine: may result in increased exposure to nifedipine when co-administered.
  • HIV protease inhibitors (indinavir, nelfinavir, ritonavir, saquinavir, or amprenavir): may result in increased exposure to nifedipine when co-administered.
  • Nefazodone: may result in increased exposure to nifedipine when co-administered.
  • Phenobarbital: reduce the bioavailability and efficacy of nifedipine
  • Phenytoin: reduce the bioavailability and efficacy of nifedipine
  • Quinidine: may result in increased exposure to nifedipine when co-administered.
  • Rifampicin: reduce the bioavailability and efficacy of nifedipine
  • Beta blockers: there have been occasional literature reports suggesting that the combination nifedipine and beta-adrenergic blocking drugs may increase the likelihood of congestive heart failure, severe hypotension or exacerbation of angina in patients with cardiovascular disease. Clinical monitoring is recommended and a dose adjustment of nifedipine should be considered.
  • Doxazosin: Compared to nifedipine monotherapy, blood pressure was lower in the presence of doxazosin. Blood pressure should be monitored when doxazosin is co-administered with nifedipine, and dose reduction of nifedipine considered.
  • Coumarin anticoagulants: There have been rare reports of increased prothrombin time in patients taking coumarin anticoagulants to whom nifedipine was administered. However the relationship to nifedipine therapy is uncertain.
  • St. John’s Wort: reduce the bioavailability and efficacy of nifedipine


Nifedipine, is rapidly and almost completely absorbed. The systemic availability of orally administered Nifedipine is 45-68% owing to a first-pass effect. Simultaneous food intake leads to delayed, but not reduced absorption.

Nifedipine is about 95% bound to plasma protein (albumin).

Nifedipine, is almost completely metabolised in the liver, primarily by oxidative processes. The metabolites show no pharmacodynamic activity.

Nifedipine is excreted in the form of its metabolites, predominantly via the kidneys; about 5-15% are excreted via the bile in the feces. The unchanged substance is recovered only in traces (below 1%) in the urine.

The terminal elimination half-life is 5.9-10.8 hours. No accumulation of the substance after the usual dose has been reported during long-term treatment. In cases of impaired kidney function, no substantial changes have been detected in comparison with healthy volunteers.

In cases of impaired liver function, the elimination half-life is distinctly prolonged and the total clearance is reduced. A dose reduction may be necessary in severe cases.



Nifedipine is usually well tolerated. Most side effects are results of vascular dilation and are generally not serious and rarely require discontinuation of therapy or dosage adjustment. They are usually transient and limited to the drug adaptation period, disappearing with the continuation of treatment.

Headaches, weakness, tiredness, reddening of face and skin, and a sensation of heat can occur, particularly at the start of treatment.

The occurrence of tachycardia, palpitations and paraesthesias has been reported.

Peripheral oedema, because of vasodilatation, particularly of the lower limbs, may occasionally develop. This appears to be dose-related and has occurred in about 1 in 25 patients at doses of less than 60 mg/day, and in about 1 in 8 patients taking 120 mg/day or more.

A mild to moderate fall in blood pressure to below normal (hypotensive circulatory reaction) may occasionally occur. This seldom requires discontinuation of therapy. This transient hypotensive effect also appears to be dose-related, and has occurred in 1 in 50 patients taking less than 60 mg/day, and in 1 in 20 patients at doses of 120 mg/day or more.

Very rarely, Nifedipine therapy has been associated with an increase in anginal pain, possibly due to associated hypotension.

Nausea, diarrhea, constipation, cramps, flatulence, allergic hepatitis.

Nasal and chest congestion, shortness of breath.

Central Nervous System
Dizziness, light-headedness, nervousness, sleep disturbances, blurred vision, equilibrium disturbances.

Dermatitis, rash, pruritus, urticaria, exanthema, and isolated cases of exfoliative dermatitis.

Rare cases of thrombocytopenia, anaemia, Leukopenia, purpura.

Rare cases of gum alterations (gingival hyperplasia), which regress completely on discontinuation of treatment.

Muscle cramps, joint stiffness, tremor, myalgia.

Fever, chills, sweating, sexual difficulties (in rare cases). In isolated cases, an initial hyperglycemic has been observed.

Rare cases of gynecomastia have been observed in older men on long-term therapy. The gynecomastia regressed completely upon discontinuation of the drug.
A slight, transient change in optical perception has occurred in individual cases, particularly after high doses.

An increase in daily urine excretion, which may be medically desirable in hypertensives, can also occur.
Disturbances of liver function (transaminase increases, intrahepatic cholestasis) may occur in individual cases. These regress after discontinuation of the drug.


Calcium Channel Blockers Pharmacology


ACE inhibitors Benazepril (Lotensin)   Captopril (Capoten)   Cilazapril   Delapril   Enalapril (Renitec, Vasotec)   Fosinopril (Monopril)  Lisinopril (Prinivil, Zestril)   Moexipril (Univasc)  Perindopril (Aceon)  Quinapril (Accupril)  Ramipril (Altace, Triatec)   Trandolapril (Mavik)  Zofenopril (Bifril, Zopranol)
Angiotensin II receptor antagonist Azilsartan (Edarbi)   Candesartan (Atacand)   Eprosartan (Teveten)   Irbesartan (Aprovel, Avapro, Karvea)   Losartan (Cozaar)   Olmesartan (Benicar, Olmetec)   Telmisartan (Micadis)   Valsartan (Diovan, Tareg)
Renin inhibitors Aliskiren (Rasilez, Tekturna)
Alpha-1 blockers Doxazosin (Cardura)   Prazosin (Minipress)   Terazosin (Hytrin)
Alpha-2 agonists (centrally acting) Clonidine (Oral route)   Clonidine (Transdermal) (Catapresan)   Guanfacine (Tenex)   Methyldopa (Aldomet)
Calcium channel blockers Dihydropyridines‎ Amlodipine (Norvasc)   Barnidipine (Vasexten)   Felodipine (Plendil)   Isradipine (Dynacirc)   Lacidipine (Lacipil, Motens)   Lercanidipine (Zanidip)   Manidipine   Nicardipine   Nifedipine (Adalat)   Nisoldipine   Nitrendipine
Benzothiazepine‎ Diltiazem (Cardizem, Taztia XT, Tiazac, Tildiem)
Phenylalkylamine‎ Gallopamil   Verapamil (Calan)
Beta blockers Beta1 selective (cardioselective) Acebutolol (Sectral)   Atenolol (Tenormin)   Betaxolol (Kerlon)   Bisoprolol (Concor)   Celiprolol (Cordiax)   Metoprolol (Betaloc, Lopressor, Toprol-XL)   Nebivolol (Bystolic, Lobivon, Nebilox)
Nonselective (Beta1 and Beta2 blockers) Oxprenolol (Trasitensin)   Propranolol (Inderal)   Timolol (Blocadren)
Nonselective (Beta1, Beta2 and Alpha1 blockers) Carvedilol (Dilatrend)   Labetalol (Trandate)
Beta blocker with intrinsic sympathomimetic activity (ISA) Acebutolol (Sectral)   Celiprolol (Cordiax)
Lipophilic Beta blockers Propranolol (Inderal)   Metoprolol (Betaloc, Lopressor, Toprol-XL)   Oxprenolol (Trasitensin)
Diuretics Carbonic anhydrase inhibitors Acetazolamide (Diamox)
Loop diuretics Bumetanide   Etacrynic acid   Furosemide (Lasix)   Piretanide   Torasemide (Demadex)
Thiazide diuretics Chlorothiazide (Diuril)   Hydrochlorothiazide (Esidrex)
Thiazide-like diuretics Chlortalidone (Hygroton)   Indapamide (Lozol, Lozide)   Metolazone
Potassium-sparing diuretics Epithelial sodium channel blockers: Amiloride (Midamor)   Triamterene (Dyrenium)
Aldosterone receptor antagonists: Potassium canrenoate   Eplerenone (Inspra)   Spironolactone (Aldactone)
Osmotic diuretics Mannitol
Combination therapy Amiloride/Hydrochlorothiazide (Moduretic)   Spironolactone/Hydrochlorothiazide (Aldactazide)
Antimigraine preparations
5 HT1 agonists (Triptans) Almotriptan (Almogran, Axert)   Eletriptan (Relpax)   Frovatriptan (Frova, Migard, Menatriptan)   Rizatriptan (Maxalt)   Sumatriptan (Imigran)   Zolmitriptan (Zomig)
Ergot alkaloids Dihydroergotamine   Ergotamine
NSAIDs/ Analgesics Indometacin   Acetylsalicylic acid (Aspirin)   Diclofenac (Voltaren)   Ibuprofen (Advil, Brufen, Dolgit, Nurofen)   Ketorolac (Toradol)   Naproxen (Naprosyn, Aleve)   Nimesulide   Paracetamol (Efferalgan, Panadol...)
Prophylaxis Cinnarizine (Stugeron, Stugeron forte)   Flunarizine (Sibelium)   Nifedipine (Adalat)   Pizotifen   Propranolol (Inderal)   Topiramate (Topamax)