Na⁺/Ca²⁺ exchange currents and SR Ca²⁺ contents in postinfarction myocytes

Myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) had lower peak cytosolic free Ca²⁺ concentration ([Ca²⁺]_i) and reduced maximal extent of cell shortening during contraction, but Ca²⁺ entry via L-type Ca²⁺ channels was normal. In the current study using whole cell patchclamp technique, reverse Na⁺/Ca²⁺ exchange current (I_Na/ca; 3 Na⁺ out:1Ca²⁺ in) was measured in myocytes in which Na⁺, K⁺, and Ca²⁺ currents were blocked or minimized. Steady-state outward currents measured under these conditions increased with depolarization or with elevation of extracellular Ca²⁺ concentration ([Ca²⁺]_o) from 1.8 to 5.0 mM, but were inhibited by 5 mM Ni²⁺ or by reduction of [Ca²⁺]_i to near zero. In addition, reduction of cytosolic free Na⁺ concentration or of [Ca²⁺]_i also decreased the amplitude of the outward current. These characteristics indicate the outward current was I_Na/Ca operating in reverse mode. Reverse I_Na/Ca was significantly lower in MI myocytes, especially at more positive voltages. In addition, sarcoplasmic reticulum (SR)-releasable Ca²⁺ content as estimated by integrating forward I_Na/Ca during caffeine-induced SR Ca²⁺ release was also significantly lower in MI myocytes. Depressed Na⁺/Ca²⁺ exchange activity may contribute to abnormal [Ca²⁺]_i dynamics in MI myocytes.