SALT INFORMATIONAmlodipine (5mg) TYPICAL USAGE Mild to moderate hypertension. Angina pectoris. Prinzmetals angina. SIDE EFFECTS Headache, peripheral oedema, fatigue, somnolence, nausea, abdominal pain, flushing, dyspepsia, palpitations, dizziness. Rarely pruritus, rash, dyspnoea, asthenia, muscle cramps. Potentially Fatal: Hypotension, bradycardia, conductive system delay and CCF. DRUG INTERACTION Increased metabolism with rifampin. Reduced hypotensive effect with calcium. Potentiates effects of thiazide diuretics and ACE inhibitors. Avoid combination with ?-blockers in patients with markedly impaired left ventricular function. May increase serum levels of CYP1A2 substrates e.g. aminophylline, fluvoxamine, ropinirole. CYP3A4 inhibitors (e.g. clarithromycin, doxycycline, isoniazid, nicardipine) may increase the effects of amlodipine. Additive BP-lowering effects when used with sildenafil, tadalafil or vardenafil. MECHANISM OF ACTION Amlodipine relaxes peripheral and coronary vascular smooth muscle. It produces coronary vasodilation by inhibiting the entry of Ca ions into the voltage-sensitive channels of the vascular smooth muscle and myocardium during depolarisation. It also increases myocardial O2 delivery in patients with vasospastic angina. Atorvastatin(10mg) TYPICAL USAGE Familial hypercholesterolaemia, homozygous familial hypercholesterolemia, hypercholesterolaemia, hyperlipoproteinaemia, hypertriglyceridaemia. SIDE EFFECTS Flatulence, weakness, headache, diarrhea, fever, myalgia, constipation, insomnia, abdominal pain, skin rashes, blurred vision, pharyngitis, dyspepsia, malaise, asthenia, arthralgia, elevation of liver enzymes, myopathy, backache, increased intracranial pressure, GI disturbance, sinusitis. DRUG INTERACTION Atorvastatin is known to interact with other drugs like aliskiren, amprenavir, cimetidine (HCl), colestipol (HCl), cyclosporin A, digoxin, erythromycin, mibefradil (Di HCl), nicotinic acid, repaglinide, warfarin (Na). Always consult your physician for the change of dose regimen or an alternative drug of choice that may strictly be required. MECHANISM OF ACTION Atorvastatin selectively and competitively inhibits the hepatic enzyme HMG-CoA reductase. As HMG-CoA reductase is responsible for converting HMG-CoA to mevalonate in the cholesterol biosynthesis pathway, this results in a subsequent decrease in hepatic cholesterol levels.