Amlodipine

Q: To which pharmacological group and subgroup does amlodipine belong?

Calcium channel blockers — a group of myotropic agents including selective L-type slow calcium channel blockers.Dihydropyridines — a subgroup of dihydropyridine derivatives with predominant effects on resistance vessels and arterial smooth muscle.

Q: What is the mechanism of action of amlodipine at the cellular level?

Calcium channel blockade — selective inhibition of voltage-gated L-type calcium channels in vascular myocytes of resistance vessels.Ion influx impairment — prevention of the transmembrane influx of calcium ions into vascular smooth muscle cells.Vasodilatation — reduction of arterial smooth muscle tone, decrease in total peripheral vascular resistance, and lowering of blood pressure.

Q: How is amlodipine metabolized and excreted from the body?

Metabolism — drug biotransformation occurs in the liver, yielding inactive metabolites.Elimination — excretion is primarily renal (about 10% unchanged and 60% as metabolites).Half-life — prolonged $T_{1/2}$ of 35–50 hours, allowing for once-daily administration.

Amlodipinum

For medical students2 min readUpdated 2026-10-10

Amlodipine is a long-acting dihydropyridine derivative used for the systematic treatment of hypertension and angina. Due to its outstanding pharmacokinetic properties, it is prescribed only once daily.

Bioavailability64–80% orally

Half-life35–50 hours ($T_{1/2}$)

Dosing RegimenOnce daily

Specific SymptomAnkle edema

General Overview and Classification

Amlodipine (also known by the trade name Norvasc) belongs to the group of dihydropyridine derivatives. In terms of its basic mechanism of action and spectrum of potential adverse reactions, this drug is largely similar to classic nifedipine, but possesses fundamentally different temporal characteristics of effect.

Pharmacokinetic Profile

The drug demonstrates excellent gastrointestinal absorption rates, surpassing many similar agents with a bioavailability of 64–80%.

Protein binding: reaches very high values at 97.5%.
Dynamics: maximum concentration ($C_{max}$) in the blood is reached 6–12 hours after administration.
Steady-state concentration: established after 7–8 days of regular use.
Metabolism and excretion: biotransformation occurs in the liver to form inactive metabolites. About 10% of the substance is excreted by the kidneys unchanged, and 60% as metabolites.

Clinical Use and Dosing

The main pharmacokinetic feature of amlodipine is its prolonged action. The elimination half-life ($T_{1/2}$) ranges from 35 to 50 hours. This exact characteristic allows the drug to be used in a convenient regimen—strictly once daily.

Direct indications for prescription include:

Systematic therapy of essential hypertension.
Treatment of angina pectoris.

Tolerability and Side Effects

In clinical practice, amlodipine is generally well tolerated by patients. However, the following adverse reactions may occur during treatment:

Specific symptom — ankle edema.
Reflex tachycardia.
Headache, dizziness, and generalized somnolence.
Nausea.

Drug Analogs

Other members of the dihydropyridine group share similar pharmacological properties. Close analogs include:

Felodipine
Lacidipine

Mnemonic

Amlodipine is the long-living dihydropyridine: a half-life ($T_{1/2}$) of 35–50 hours allows for a dosing frequency of just once daily, but remember its hallmark side effect — ankle edema.

Frequently asked questions

To which pharmacological group and subgroup does amlodipine belong?

Calcium channel blockers — a group of myotropic agents including selective L-type slow calcium channel blockers.
Dihydropyridines — a subgroup of dihydropyridine derivatives with predominant effects on resistance vessels and arterial smooth muscle.

What is the mechanism of action of amlodipine at the cellular level?

Calcium channel blockade — selective inhibition of voltage-gated L-type calcium channels in vascular myocytes of resistance vessels.
Ion influx impairment — prevention of the transmembrane influx of calcium ions into vascular smooth muscle cells.
Vasodilatation — reduction of arterial smooth muscle tone, decrease in total peripheral vascular resistance, and lowering of blood pressure.

How is amlodipine metabolized and excreted from the body?

Metabolism — drug biotransformation occurs in the liver, yielding inactive metabolites.
Elimination — excretion is primarily renal (about 10% unchanged and 60% as metabolites).
Half-life — prolonged $T_{1/2}$ of 35–50 hours, allowing for once-daily administration.

What is the pathogenesis of specific ankle edema development during amlodipine therapy?

Detailed pathogenesis regarding the development of specific ankle edema is not elaborated in the source texts, which only mention the occurrence of this adverse effect.

What are the absolute contraindications to amlodipine?

Sources note an absolute contraindication: ALT levels exceeding 2.5 times the upper limit of normal.
Limitations and unfavorable clinical scenarios also include chronic heart failure and therapy with high doses of insulin or its analogs; amlodipine therapy is not recommended in NASH.

What is the half-life of amlodipine and how does it affect the dosing regimen?

The half-life ($T_{1/2}$) of amlodipine ranges from 35 to 50 hours. Due to its prolonged presence in the body, the drug is prescribed to patients once daily.

What specific side effect is characteristic of amlodipine?

A specific and characteristic symptom when taking amlodipine is ankle edema. Headache, reflex tachycardia, and nausea may also occur.

What drugs are analogs of amlodipine?

Analogs with similar pharmacological properties include felodipine and lacidipine.

Go deeper

Comparison of bioavailability and plasma protein binding between amlodipine and nifedipine
Dynamics of achieving steady-state plasma concentrations
Hepatic metabolic pathways of amlodipine and the role of the kidneys in metabolite elimination
Pathogenesis of reflex tachycardia and ankle edema induced by dihydropyridines
Clinical differences in the use of felodipine and lacidipine