Xq. Zhang et al., NA+ CA2+ EXCHANGE CURRENTS AND SR CA2+ CONTENTS IN POSTINFARCTION MYOCYTES/, American journal of physiology. Cell physiology, 40(6), 1996, pp. 1800-1807
Myocytes isolated from rat hearts 3 wk after myocardial infarction (MI
) had lower peak cytosolic free Ca2+ concentration ([Ca2+](i)) and red
uced maximal extent of cell shortening during contraction, but Ca2+ en
try via L-type Ca2+ channels was normal. In the current study using wh
ole cell patch-clamp technique, reverse Na+/Ca2+ exchange current (I-N
a/Ca; 3 Na+ out:1 Ca2+ in) was measured in myocytes in which Na+, K+,
and Ca2+ currents were blocked or minimized. Steady-state outward curr
ents 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 Naf concent
ration or of [Ca2+](i) also decreased the amplitude of the outward cur
rent. These characteristics indicate the outward current was I-Na/Ca o
perating in reverse mode. Reverse I-Na/Ca was significantly lower in M
I myocytes, especially at more positive voltages. In addition, sarcopl
asmic reticulum (SR)-releasable Ca2+ content as estimated by integrati
ng forward I-Na/Ca during caffeine-induced SR Ca2+ release was also si
gnificantly lower in MI myocytes. Depressed Na+/Ca2+ exchange activity
may contribute to abnormal [Ca2+](i) dynamics in MI myocytes.