Na+-ca2+ exchange currents and sr ca2+ contents in post-infarction
myocytes.
Zhang, Xue-Qian, Douglas L. Tillotson, Russell L. Moore, R. Zelis, and
Joseph Y. Cheung.
Departments of Medicine, and Cellular and Molecular Physiology,
Milton S. Hershey Medical Center, Pennsylvania State University,
Hershey, PA 17033; Department of Kinesiology, University of Colorado,
Boulder, CO 80309; and Department of Physiology, Boston University
School of Medicine, Boston, MA 02188
APStracts 3:0206C, 1996.
Myocytes isolated from rat hearts 3 weeks post myocardial infarction
(MI) have lower peak cytosolic 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 patch clamp, reverse INaCa (3Na+ out, 1 Ca2+ 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 elevating
extracellular Ca2+ concentration ([Ca2+]o) from 1.8 to 5.0mM; but
inhibited by 5mM Ni2+ or by reducing [Ca2+]i to close to zero. In
addition, reducing [Na+]i or [Ca2+]i also decreased the amplitude of
the outward current. These characteristics indicate the outward
current was INaCa operating in reverse mode. Reverse INaCa was
significantly lower in MI myocytes, especially at more positive
voltages. In addition, SR releasable Ca2+ content as estimated by
integrating forward INaCa 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.
Received 20 November 1995; accepted in final form 19 June 1996.
APS Manuscript Number C700-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 4 July 96