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5 Cards in this Set
- Front
- Back
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MECHANISM
Nitrates |
Denitration of the nitrates within smooth muscle cells releases nitric oxide (NO), which stimulates guanylyl cyclase, and causes an increase of the second messenger cGMP (cyclic guanosine monophosphate); the latter results in smooth muscle relaxation by dephosphorylation of myosin light chain phosphat
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MECHANISM
Calcium Channel-Blocking Drugs |
Calcium channel blockers block voltage-gated L-type calcium channels, the calcium channels most important in cardiac and smooth muscle. By decreasing calcium influx during action potentials in a frequency- and voltage-dependent manner, these agents reduce intracellular calcium concentration and muscle contractility
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MECHANISM
Beta-Blocking Drugs |
These drugs are described in detail in Chapter 10. Because they reduce cardiac work (and oxygen demand), all blockers are effective in the prophylaxis of atherosclerotic angina attacks.
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Ranolazine
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Ranolazine appears to act mainly by reducing a late, prolonged sodium current in myocardial cells. The decrease in intracellular sodium causes an increase in calcium expulsion via the Na/Ca transporter (see Chapter 13) and a reduction in cardiac force and work. As noted previously, it may also alter cardiac metabolism. Ranolazine is moderately effective in angina prophylaxis
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Ivabradine
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Ivabradine inhibits the If sodium current in the sinoatrial node. The reduction in this hyperpolarization-induced inward pacemaker current results in decreased heart rate and consequently decreased cardiac work. If approved, it will probably be used only for prophylaxis.
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