Lercanidipine

Lercanidipine is an antihypertensive, a blood pressure-lowering drug. It is from the dihydropyridine class of calcium channel blockers. These drugs work by relaxing and opening the blood vessels. This allowing the blood to circulate more freely around the body. As a result, the blood pressure lowers and allows the heart to work more efficiently. It is recommended for patients with high blood pressure as taking Lercanidipine helps prevent heart disease, heart attacks and strokes. Lercanidipine is sold under various commercial names including Zanidip. But due to global demand, this medicine is manufactured and sold around the world by global and local manufacturers and marketers. Recordati S.A., Chemical And Pharmaceutical Company patented Lercanidipine in 1984 and it was approved for medical use in 1997.

Forms and dose:

Lercanidipine is sold as tablet available in two strengths of 10 mg and 20 mg. The initial dose starts with 10 mg daily, however, the doctor can increase the dose to 20 mg daily, if the initial dose has not produced the desired reduction in symptoms. Lercanidipine is taken tablet with a drink of water and most people take it before the morning breakfast. It should be taken on an empty stomach about 30 minutes before a meal.

The price of Lercanidipine

In the USA, The lowest price consumers pay for Lercanidipine 20 mg is $0.81 per pill or unit for 90 pills. Whereas in the UK, 28 tabs of 10mg will cost the consumers $53.73.

How does it work?

As a dihydropyridine class calcium channel blockers, its actions block L-type calcium channels in the smooth muscle cells of blood vessels. Lercanidipine inhibits the influx of extracellular calcium across the myocardial and vascular smooth muscle cell membranes possibly by deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum. The depletion of intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, leading to dilation of the coronary and systemic arteries. Causing increased oxygen delivery to the myocardial tissue decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload. In contrast to the non-dihydropyridine calcium channel blockers, it does not significantly act on calcium channels in the atrioventricular node, thus does not decrease heart rate. It gets quickly distributed into the tissues and bound to lipid membranes, where it forms a depot.

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