Nifedipin T20 Retard Mechanism of Action

Pharmacology: Pharmacodynamics: Nifedipine is a calcium antagonist of the 1,4-dihydropyridine type. Calcium antagonists reduce the transmembranal influx of calcium ions through the slow calcium channel into the cell. As a specific and potent calcium antagonist, nifedipine acts particularly on the cells of the myocardium and the smooth muscle cells of the coronary arteries and the peripheral resistance vessels. The main action of nifedipine is to relax arterial smooth muscle, both in the coronary and peripheral circulation.
In hypertension, the main action of nifedipine is to cause peripheral vasodilatation and thus reduce peripheral resistance.
In angina, nifedipine reduces peripheral and coronary vascular resistance, leading to an increase in coronary blood flow, cardiac output and stroke volume, whilst decreasing after-load. Additionally, nifedipine dilates submaximally both clear and atherosclerotic coronary arteries, thus protecting the heart against coronary artery spasm and improving perfusion to the ischaemic myocardium.
Pharmacokinetics: Nifedipine is rapidly and almost completely absorbed from the gastrointestinal tract, but undergoes extensive hepatic first-pass metabolism. Nifedipine is about 92% to 98% bound to plasma proteins. It is distributed into breast milk. It is extensively oxidised in the liver and 80% to 95% of a dose is excreted in the urine, and the remainder in the faeces, almost entirely as inactive metabolites. The terminal half-life following longer-acting formulations administration does not represent a meaningful parameter as a plateau-like plasma concentration is maintained during release from the tablets and absorption.