From where it gets absorbed into body ,Please,can you give details about A.D.M.E. of Atrovastatin .
What is the mechanism of action of Atrovastatin ?
- 25 Dec 2009 by Mukhtar75
- 1 January 2010
I will be honest I can not answer your question. But !! Yes, I said But!! Have you looked on Google Scholar. You go to the Google search engine and type in Google Scholar then wriite in what you are looking for it should be there.
I do wish you the best. If I come across anything I will let you know.
Mechanism of Action
LIPITOR is a selective, competitive inhibitor of HMG-CoA reductase, the
rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl-coenzyme A
to mevalonate, a precursor of sterols, including cholesterol. Cholesterol
and triglycerides circulate in the bloodstream as part of lipoprotein complexes.
With ultracentrifugation, these complexes separate into HDL (highdensity
lipoprotein), IDL (intermediate-density lipoprotein), LDL (low-density
lipoprotein), and VLDL (very-low-density lipoprotein) fractions. Triglycerides and released into the plasma for delivery to peripheral tissues. LDL is formed from VLDL and is catabolized primarily through the high-affinity LDL receptor. Clinical and pathologic studies show that elevated plasma levels of total cholesterol (total-C), LDL-cholesterol (LDL-C), and apolipoprotein B (apo B) promote human atherosclerosis and are risk factors for developing cardiovascular disease, while increased levels of HDL-C are associated with a decreased cardiovascular risk.In animal models, LIPITOR lowers plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of hepatic LDL receptors on the cell surface to enhance uptake and catabolism of LDL; LIPITOR also reduces LDL production and the number of LDL particles. LIPITOR reduces LDL-C in some patients with homozygous familial hypercholesterolemia (FH), a population that rarely responds to other lipid-lowering medication(s).
A variety of clinical studies have demonstrated that elevated levels of total-C, LDL-C, and apo B (a membrane complex for LDL-C) promote human atherosclerosis.
Similarly, decreased levels of HDL-C (and its transport complex,
apo A) are associated with the development of atherosclerosis. Epidemiologic investigations have established that cardiovascular morbidity and mortality vary directly with the level of total-C and LDL-C, and inversely with the level of HDL-C. LIPITOR reduces total-C, LDL-C, and apo B in patients with homozygous and heterozygous FH, nonfamilial forms of hypercholesterolemia, and mixed dyslipidemia. LIPITOR also reduces VLDL-C and TG and produces variable increases in HDL-C and apolipoprotein A-1. LIPITOR reduces total-C,
LDL-C, VLDL-C, apo B, TG, and non-HDL-C, and increases HDL-C in patients with isolated hypertriglyceridemia. LIPITOR reduces intermediate density lipoprotein cholesterol (IDL-C) in patients with dysbetalipoproteinemia.
Like LDL, cholesterol-enriched triglyceride-rich lipoproteins, including
VLDL, intermediate density lipoprotein (IDL), and remnants, can also promote atherosclerosis. Elevated plasma triglycerides are frequently found in a triad with low HDL-C levels and small LDL particles, as well as in association with non-lipid metabolic risk factors for coronary heart disease. As such, total plasma TG has not consistently been shown to be an independent risk factor for CHD. Furthermore, the independent effect of raising HDL or lowering TG on the risk of coronary and cardiovascular morbidity and mortality has not been determined.
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