t is a selective, competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme responsiblefor the conversion of 3- hydroxy- 3- methyl- glutaryl- coenzyme A to mevalonate, a precursor of sterols,including cholesterol. Triglycerides (TG) and cholesterol in the liver are incorporated into VLDL andreleased into the plasma for delivery to peripheral tissues. Low-density lipoprotein (LDL) is formed from VLDL and is catabolized primarily through the high affinity LDL receptor.

Atorvastatin lowers plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase andcholesterol synthesis in the liver and increases the number of hepatic LDL receptors on the cell surfacefor enhanced uptake and catabolism of LDL. It reduces LDL production and the number of LDL particles. It produces a profound and sustained increase in LDL receptor activity coupled with abeneficial change in the quality of circulating LDL particles.