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Background —The Na+ /Ca2+ exchange (NCX) extrudes Ca2+ from cardiac myocytes, but it can also mediate Ca2+ influx, load the sarcoplasmic reticulum with Ca2+ , and trigger Ca2+ release from the sarcoplasmic reticulum. In ischemia/reperfusion or digitalis toxicity, increased levels of intracellular [Na+ ] ([Na+ ]i ) may raise levels of intracellular [Ca2+ ] ([Ca2+ ]i ) via NCX, leading to cell injury and arrhythmia.Methods and Results —We used KB-R7943 (KBR) to selectively block Ca2+ influx via NCX to study the role of NCX-mediated Ca2+ influx in intact rat ventricular myocytes. Removing extracellular Na+ caused [Ca2+ ]i to rise, due to Ca2+ influx via NCX, and this was blocked by 90% with 5 μmol/L KBR. However, KBR did not alter [Ca2+ ]i decline due to NCX. Thus, we used 5 μmol/L KBR to selectively block Ca2+ entry but not efflux via NCX. Under control conditions, 5 μmol/L KBR did not alter steady-state twitches, Ca2+ transients, Ca2+ load in the sarcoplasmic reticulum, or rest potentiation, but it did prolong the late low plateau of the rat action potential. When Na+ /K+ ATPase was inhibited by strophanthidin, KBR reduced diastolic [Ca2+ ]i and abolished the spontaneous Ca2+ oscillations, but it did not prevent inotropy.Conclusions —In rat ventricular myocytes, Ca2+ influx via NCX is not important for normal excitation-contraction coupling. Furthermore, the inhibition of Ca2+ efflux alone (as [Na+ ]i rises) may be sufficient to cause glycoside inotropy. In contrast, Ca2+ overload and spontaneous activity at high [Na+ ]i was blocked by KBR, suggesting that net Ca2+ influx (not merely reduced efflux) via NCX is involved in potentially arrhythmogenic Ca2+ overload.

circulation

KB-R7943 Block of Ca 2+ Influx Via Na + /Ca 2+ Exchange Does Not Alter Twitches or Glycoside Inotropy but Prevents Ca 2+ Overload in Rat Ventricular Myocytes