Possible Interaction: Ranolazine and Calcium Supplement

“More ecent evidence suggests that ranolazine prevents ischemiaelated calcium and sodium overload by blocking the late odium current.”

“ Ranolazine reduces Na overload induced by calcium and improves diastolic relaxation and coronary subendocardial flow, without affecting hemodynamic parameters such as blood pressure, heart rate, or inotropic state of the heart, avoiding undesirable side effects.”

“ Ranolazine thereby reduces intracellular sodium and calcium accumulation during ischemia, as shown in various animal research models.”

“ Ranolazine , a selective inhibitor of the late sodium current, can reduce sodium accumulation and Ca 2 + overload.”

“ Ranolazine inhibits sodium voltage-dependent channels, suggesting their possible involvement in the reperfusion process by preventing the sodium and calcium overload that occurs during ischemia.”

“ Ranolazine (10 μM), but not lidocaine (10 μM), reduced RM NCX1.1-mediated Ca2+i overload in ventricular myocytes.”

“ Ranolazine and lidocaine (10 μM) similarly reduced Ca2+i overload and improved left ventricle work recovery in whole-heart models of IR injury or exposure to ouabain (80 μM).”

“ Ranolazine may provide functional protection of the heart during IR injury by reducing cCa2+ and mCa2+ loading secondary to its effect to block the late Na+ current.”

“Reduction by RAN of INa,L-induced dysregulation of calcium cycling could contribute to the antiarrhythmic actions of this agent in both reentrant and triggered arrhythmias.”

“In working hearts, 10 micromol/L ranolazine significantly increased glucose oxidation 1.5-fold to 3-fold under conditions in which the contribution of glucose to overall ATP production was low (low Ca , high FA, with insulin), high (high Ca, low Fa, with pacing), or intermediate.”

“ Ranolazine induces in fact a reduction of the intracellular late sodium current that leads to a reduction of the intracellular calcium concentration thus producing a better myocardial diastolic relaxation process which in its turns enhances the myocardial perfusion.”