Adalat GITS 30 Mechanism of Action

Antianginal/Antihypertensive.
Nifedipine is a calcium antagonist of the 1,4-dihydropyridine type. Calcium antagonists reduce the transmembrane influx of calcium ions through the slow calcium channel into the cell. Nifedipine acts particularly on the cells of the myocardium and the smooth muscle cells of the coronary arteries and the peripheral resistance vessels.
In the heart, nifedipine dilates the coronary arteries, especially the large conductance vessels, even in the free wall segment of partially stenosed areas. Further, nifedipine reduces the vascular smooth muscle tone in the coronary arteries and prevents vasospasm. The end-result is an increased post-stenotic blood flow and an increased oxygen supply. Parallel to this, nifedipine reduces the oxygen requirement by lowering peripheral resistance (afterload). With long-term use, nifedipine can also prevent the development of new atherosclerotic lesions in the coronary arteries.
Nifedipine reduces the smooth muscle tone of the arterioles, thus lowering the increased peripheral resistance and consequently, the blood pressure. At the beginning of the nifedipine treatment, there may be a transient reflex increase in heart rate, and thus in the cardiac output. However, this increase is not enough to compensate for the vasodilation. In addition, nifedipine increases sodium and water excretion both in the short- and long-term use. The blood pressure-lowering effect of nifedipine is particularly pronounced in hypertensive patients.
Adalat GITS 30 tablets are formulated to provide nifedipine at an approximately constant rate over 24 hrs. Nifedipine is released from the tablet at a zero-order rate by a membrane-controlled, osmotic push-pull process. The delivery rate is independent of gastrointestinal pH or motility. Upon swallowing, the biologically inert components of the tablet remain intact during gastrointestinal transit and are eliminated in the feces as an insoluble shell.