Atorvastatin calcium is an artificial lipid-lowering agent that catalyzes the transformation of HMG-CoA to mevalonate, a rate-limiting and initial step in the biosynthesis of cholesterol. This enzyme is an off-white to white crystalline fine particles, which is somewhat very soluble in phosphate buffer of pH7.4, acetonitrile, distilled water, and ethanol, as well as being generously methanol soluble.
In humans, atorvastatin calcium and a number of its metabolites are active pharmacologically. Its main site of action, as well as the foremost cholesterol synthesis site and LDL clearance, is the liver. The dosage of drug rather than the systemic drug concentration associates superiorly with LDL clearance.
Atorvastatin calcium functions by obstructing an enzyme inside the liver, which the body utilizes to produce cholesterol. Once smaller amounts of cholesterol are created, the liver gets more cholesterol from bloodstreams, resulting to lower cholesterol level that circulates in the blood. Triglycerides and cholesterol flow in bloodstreams as fractions of lipoprotein complexes. Through the process of ultracentrifugation, these lipoprotein complexes divide into high-density lipoprotein (HDL), low-density lipoprotein (LDL), intermediate-density lipoprotein (IDL), and very-low-density lipoprotein (VLDL) parts.
Inside the liver, cholesterol and triglycerides are integrated into VLDL, freed into the plasma, and distributed to the peripheral tissues. LDL is produced from VLDL and catabolized mainly through high-affinity LDL receptor. Pathological and clinical researches explain that high plasma levels of total-C (total cholesterol), LDL cholesterol, and apolipoprotein B, encourage atherosclerosis in humans and are threat factors in increasing cardiovascular disease, at the same time as amplified HDL cholesterol levels are connected with a reduction of cardiovascular risk.
Atorvastatin calcium reduces lipoprotein levels and plasma cholesterol through slowing down HMG-CoA reductase and the synthesis of cholesterol inside the liver, and increasing the hepatic number of LDL receptors in the surface of the cell to improve LDL catabolism and uptake. It also lessens the production of LDL and several LDL particles. It also produces a constant and noticeable increase in the activity of LDL receptor joined with an advantageous change in superiority of flowing LDL particles.
Various clinical and pathologic investigations shows that atorvastatin calcium reduced LDL-cholesterol, total-C, and apolipoprotein B in both patients with heterozygous and homozygous FH, mixed dyslipidaemia, non-familial types of hypercholesterolaemia, and normal volunteers. It has also shown to reduce triglycerides and VLDL-cholesterol, as well as producing changeable increases in apolipoprotein A-1 and HDL-cholesterol.
Atorvastatin calcium provides good benefits for the human body, particularly in lowering cholesterol. Atorvastatin calcium or Lipitor is usually well-tolerated with transient and mild adverse reactions.
In humans, atorvastatin calcium and a number of its metabolites are active pharmacologically. Its main site of action, as well as the foremost cholesterol synthesis site and LDL clearance, is the liver. The dosage of drug rather than the systemic drug concentration associates superiorly with LDL clearance.
Atorvastatin calcium functions by obstructing an enzyme inside the liver, which the body utilizes to produce cholesterol. Once smaller amounts of cholesterol are created, the liver gets more cholesterol from bloodstreams, resulting to lower cholesterol level that circulates in the blood. Triglycerides and cholesterol flow in bloodstreams as fractions of lipoprotein complexes. Through the process of ultracentrifugation, these lipoprotein complexes divide into high-density lipoprotein (HDL), low-density lipoprotein (LDL), intermediate-density lipoprotein (IDL), and very-low-density lipoprotein (VLDL) parts.
Inside the liver, cholesterol and triglycerides are integrated into VLDL, freed into the plasma, and distributed to the peripheral tissues. LDL is produced from VLDL and catabolized mainly through high-affinity LDL receptor. Pathological and clinical researches explain that high plasma levels of total-C (total cholesterol), LDL cholesterol, and apolipoprotein B, encourage atherosclerosis in humans and are threat factors in increasing cardiovascular disease, at the same time as amplified HDL cholesterol levels are connected with a reduction of cardiovascular risk.
Atorvastatin calcium reduces lipoprotein levels and plasma cholesterol through slowing down HMG-CoA reductase and the synthesis of cholesterol inside the liver, and increasing the hepatic number of LDL receptors in the surface of the cell to improve LDL catabolism and uptake. It also lessens the production of LDL and several LDL particles. It also produces a constant and noticeable increase in the activity of LDL receptor joined with an advantageous change in superiority of flowing LDL particles.
Various clinical and pathologic investigations shows that atorvastatin calcium reduced LDL-cholesterol, total-C, and apolipoprotein B in both patients with heterozygous and homozygous FH, mixed dyslipidaemia, non-familial types of hypercholesterolaemia, and normal volunteers. It has also shown to reduce triglycerides and VLDL-cholesterol, as well as producing changeable increases in apolipoprotein A-1 and HDL-cholesterol.
Atorvastatin calcium provides good benefits for the human body, particularly in lowering cholesterol. Atorvastatin calcium or Lipitor is usually well-tolerated with transient and mild adverse reactions.
