| Mechanism | Drug | Disease or Use |
| Inhibits VLDL synthesis raising HDL - largest increase in HDL, small reduction in LDL, larger reduction in triglycerides | |
| Inhibits angiotensin-converting enzyme (ACE), arterial vasodilation, reverses cardiac and arterial remodeling, reduced aldosterone secretion | |
| Accelerates inactivation of factor Xa | |
| Sources of NO in vascular smooth muscle, dilation of veins more than arteries, dilation of large not small coronary arteries | |
| Activates A1 receptors in AV node, slows conduction in the AV node, increases the effective refractory period in the AV node | |
| α1 receptor antagonist, vasodilation | |
| AT1 receptor antagonist (ARB), otherwise same as Lisinopril | |
| Prevent binding of fibrinogen to thrombin | |
| Source of NO + inhibitor of ROS production dilation of veins more than arteries, anti-remodeling activity | |
| Block sodium channels in collecting duct | |
| Blocks sodium channels, stabilizes inactivated state of sodium channels, slows conduction in the ventricles, increases the effective refractory period in the ventricles | |
| Inhibits sodium-potassium ATPase resulting in greater delivery of calcium to the contractile apparatus of cardiomyocytes, increases activity in the vagus nerve, slows conduction an | |
| Monoclonal antibody directed against GPIIb/IIIa receptor, inhibition of platelet aggregation | |
| Inhibits the carboxylation of glutamate residues in Vitamin K-dependent clotting factors | |
| Blocks intestinal transport of cholesterol, modest reduction in LDL, no change in HDL | |
| Blockers of GPIIb/IIIa receptor, inhibition of platelet aggregation | |
| Block cardiac and vascular L-type calcium channels, stabilize inactivated state of those calcium channels, arterial vasodilation, reduce inotropy and chronotropy, reduce myocardial | |
| α1β antagonist, reduces inotropy and chronotropy, vasodilation, anti-oxidant, anti-apoptotic activity | |
| Cleave fibrin to resolve clot | |
| Blocks vascular L-type calcium channels, stabilizes inactivated state of those calcium channels, reduces myocardial oxygen demand, arterial vasodilation | |
| | Mechanism | Drug | Disease or Use |
| Block potassium channels, varying effects on sodium and calcium channels, inhibit repolarization in the atria and ventricles | |
| β1 antagonist/increases NO availability, reduces inotropy and chronotropy, vasodilation, anti-remodeling activity | |
| Blocks the pacemaker channel in the SA node (HCN4), reduces heart rate without affecting inotropy or blood pressure, reduces myocardial oxygen demand | |
| Irreversible cyclo-oxygenase (1 and 2) inhibition; inhibition of platelet activation | |
| β1-selective antagonists, reduce inotropy and chronotropy, reduce myocardial oxygen demand, slow conduction and increase refractoriness in AV node, reverse cardiac and arterial re | |
| Non-selective β receptor antagonist, blocks potassium channels, slows conduction in the AV node, increases the effective refractory period in the AV node, inhibits repolarization | |
| Inhibit HMGCoA reductase, greatest reduction in LDL, little increase in HDL | |
| Activate PPARα leading to increased lipoprotein lipase activity, reduced triglyceride synthesis, increased β-oxidation of fatty acids, small reduction in LDL, larger reduction in | |
| Thrombin inhibitors | |
| Accelerates inactivation of thrombin (factor IIa) | |
| Increases osmolarity of extracellular fluid, washes out countercurrent multiplier | |
| Mineralocorticoid (aldosterone) receptor antagonists | |
| Antagonists of P2T purinergic receptor; inhibition of platelet aggregation | |
| Blocks potassium channels, inhibits repolarization in the atria and ventricles | |
| Inhibit sodium-chloride cotransport in distal tubule (elimination of Na+ and water), direct arterial vasodilation (reduced blood pressure) | |
| Bind bile acids in intestine, modest reduction in LDL, little increase in HDL | |
| Inhibition of cyclic nucleotide phosphodiesterase; inhibition of platelet activation | |
| Blocks late sodium channel, reduces inotropy without affecting heart rate or blood pressure, reduces myocardial oxygen demand | |
| Inhibits NKCC2 cotransporter in thick ascending limb, stimulates NO/prostaglandin synthesis in veins, renal afferent arteriole, and to a lesser extent in other arteries, dilation o | |
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