Ranolazine reduces angina frequency by a mechanism that differs from nitrates and beta-blockers. Its primary mechanism is:
- A Inhibition of late inward sodium current (late INa), reducing intracellular Na+ and secondary Ca2+ overload ✓
- B Activation of ATP-sensitive K+ channels causing coronary vasodilation
- C Direct blockade of L-type calcium channels in vascular smooth muscle
- D Reduction of myocardial oxygen demand by beta-1 blockade
Explanation
Ranolazine inhibits the late (sustained) component of the inward sodium current (late INa) in cardiac myocytes. This reduces intracellular Na+ accumulation; less Na+ means less Ca2+ entry via the reverse Na+/Ca2+ exchanger, reducing diastolic Ca2+ overload and improving myocardial relaxation and oxygen efficiency. Its anti-ischaemic effect occurs without significant changes in heart rate or blood pressure.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.