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Calcium Channel Antagonists Drug Verapamil (phenylalkylamine) Nifedipine Nicardipine Nimodipine Nitrendipine Isradipine Amlodipine (dihydropyridine) Diltiazem (benzothiazepine) MOA calcium channel blocking agent that inhibits the movement of calcium ions across cell membranes of arterial smooth muscle and cardiac muscle reduced influx of calcium ions results in a relaxation of arterial smooth muscle and negative inotropy reduces afterload, dilates the main coronary arteries and arterioles, and inhibits coronary artery spasm. The negative inotropic effect is offset by the decrease in afterload and a reflex increase in adrenergic tone inhibition of calcium ion movement also results in prolongation of the atrioventricular (AV) nodal effective refractory period and slowed AV conduction dihydropyridine calcium channel blocking agents selectively inhibits calcium influx across cell membranes in cardiac and vascular smooth muscle, with a greater effect on vascular smooth muscle peripheral arteriolar vasodilator; thus it reduces afterload calcium channel blocking agent that inhibits the influx of calcium ions into cell membranes of vascular smooth muscle and cardiac muscle on vascular smooth muscle results in a decrease in peripheral vascular resistance and a consequent reduction in blood pressure with a slight reduction in heart rate decreases conduction through the sinoatrial (SA) and atrioventricular (AV) nodes, produces small increases in the PR interval, and reduces the renal and peripheral effects of angiotensin II greater effect on coronary circ. than on other vascular beds Pharmacokinetics oral onset of action: 30 min. (IV - <2 min.) plasma t ½ 4-12 hr hepatic metabolism and elim. primarily renal excretion Toxicity severe heart block (if IV with beta antagonist or dig toxicity) myocardial depression hypotension if given with dig, may cause dig toxicity SE: constipation, N, dizziness, flushing, pedal edema Clinical Use SVT, A-fib, A-flutter, angina, hypertrophic cardiomyopathy, hypertension, and Raynaud’s Syndrome oral onset of action: 20 min. (sublingual – 3 min.) plasma t ½ 2-4 hr primarily renal excretion hypotension SE: dizziness, flushing, HA, palpitations, rare exacerbation of angina, pedal edema angina, hypertension, Raynaud’s Syndrome (and peripheral vascular disease) no useful antiarrhythmic properties oral onset of action: 30-60 min. plasma t ½ 3-7 hr hepatic metabolism fecal elim. bradycardia depression of AV nodal conduction SE: HA, flushing, dizziness angina, SVT, A-fib, A-flutter, hypertension, Raynaud’s Syndrome; inhibits platelet aggregation Bepridil combine potent non-calcium related effects (fast Na+ channel inhibition and inhibition of calmodulin) tx for refractory angina, but can cause life-threatening arrythmias (can prolong QT interval and can cause torsades de pointes in those with hypo-K+ Mibefradil produces coronary and peripheral vasodilation decreases heart rate, but does not decrease myocardial contractility tx of HTN and chronic stable angina the pharm. syllabus says that we are not responsible for bepridil or mebefradil