Ranolazine is used as adjunctive anti-anginal therapy. Its anti-ischemic effect is mediated by inhibition of:
- A Late inward sodium current (late INa), reducing calcium overload ✓
- B L-type calcium channels, reducing afterload
- C Beta-1 adrenoceptors, reducing oxygen demand
- D Fatty acid oxidation, shifting metabolism to glucose
Explanation
Ranolazine inhibits the late inward sodium current (late INa) that is pathologically increased during ischemia. Sodium overload via late INa triggers reverse-mode Na-Ca exchange, causing calcium overload in cardiomyocytes that leads to diastolic dysfunction and wall stiffness. By blocking late INa, ranolazine reduces intracellular calcium, improves diastolic relaxation, and decreases oxygen demand without affecting heart rate or blood pressure. It does not affect beta-receptors or L-type calcium channels significantly at therapeutic doses.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.