Abstract: Calcium channel blockers (CCBs) arrest cholesterol induced increase in membrane Ca++ permeability which inhibits Cell growth and prevent atherosclerosis in animals with Hyperlipidemia, nitric oxide production from endothelial cells, superoxide anion scavenge and ACE inhibition. EDTA does partial removal of Ca++ from atherosclerotic plaque, reduction of free radical production and lipid peroxidation, improves Ca++/Mg++ balance, reduce platelet aggregation and improve blood flow. Hence, the study was undertaken to establish the role of Ca++ on lipid profile using various CCBs and EDTA therapy in combination with Atorvastatin in Wistar Albino Rats. Group 1: Normal, 2: Control, 3: ATR, 4: Atorvastatin and Amlodipine, 5: Atorvastatin and Diltiazem, 6: Atorvastatin and Verapamil, 7: Atorvastatin and EDTA. Normal group received a standard commercial rat chow diet while other groups received a high cholesterol diet for 21 days. Atorvastatin, Amlodipine, Diltiazem, Verapamil and EDTA solutions were administered orally once daily for 21 days to respective groups. The HCD has significantly increased serum TC, TG and VLDL levels while serum HDL, LDL, HDL/LDL ratio, atherogenic index and serum calcium levels were not significantly affected in control group as compared with normal group. Atorvastatin significantly decreased serum TG, VLDL-C and serum Ca++. Atorvastatin-Amlodipine combination has significantly decreased serum TC and LDL-C as compared with control group. Atorvastatin-Diltiazem combination has significantly decreased TC and LDL-C as compared with control group and has significantly increased serum Ca++ as compared with Atorvastatin group. Atorvastatin-Amlodipine combination has significantly decreased SOD level and increased GSH and catalase level as compared with control group. In conclusion, there is no significant effect of EDTA after oral administration. So, further investigation can be done by changing the EDTA route of administration (i.e. intra venous).
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