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

Abstract

In rat ventricular myocytes, Ca(2+) influx via NCX is not important for normal excitation-contraction coupling. Furthermore, the inhibition of Ca(2+) efflux alone (as [Na(+)](i) rises) may be sufficient to cause glycoside inotropy. In contrast, Ca(2+) overload and spontaneous activity at high [Na(+)](i) was blocked by KBR, suggesting that net Ca(2+) influx (not merely reduced efflux) via NCX is involved in potentially arrhythmogenic Ca(2+) overload.