AJP - Heart and Circulatory Physiology, Vol 246, Issue 2 222-H231, Copyright © 1984 by American Physiological Society
Effect of sodium on calcium-dependent force in unstimulated rat cardiac muscle
G. D. Walford, G. Gerstenblith and E. G. Lakatta
It has previously been demonstrated that 1) changes in superfusate calcium
concentration [Ca2+]o within the low millimolar range result in changes in
"resting" force and in the light-scattering properties of unstimulated rat
cardiac muscle, and 2) if [Ca2+]o is increased from zero to millimolar
concentrations, i.e., reperfusion with Ca2+ after a Ca2+-free period, a
large influx of Ca2+ occurs and is associated with a substantial increase
in resting force. The present study determined whether the Ca2+ influx in
either case was influenced by intracellular sodium (Na+i). In unstimulated
isometric rat right ventricular papillary muscles equilibrated at 29
degrees C, [Ca2+]o was increased from 1 to 4 mM or from 0 to 2 mM under
conditions that vary Na+i, and the resulting change in intracellular
calcium concentration [( Ca2+]i) was monitored by changes in both resting
force and the frequency of intensity fluctuations in laser light scattered
by the muscle. In each case, lowering Na+i by equilibration in lowered
extracellular sodium concentration [( Na+]o) or enhancing [Na+]i by
equilibration in the absence of extracellular potassium or in the presence
of ouabain markedly lowered and enhanced respectively the apparent Ca2+
influx in response to the step increase in [Ca2+]o. Thus, in unstimulated
rat cardiac muscle, Na+i modulates the Ca2+ influx resulting from a step
increase in [Ca2+]o both under physiological conditions and following a
period of Ca2+-free superfusion, i.e., the "Ca2+ paradox." A passive influx
of Ca2+ down its electrochemical gradient would not depend on Na+i, and the
voltage-time dependent slow Ca2+o channel is inactivated under the
experimental conditions employed. The results are best explained by a
sarcolemmal Na+-Ca2+ exchange mechanism and suggest that the reversal
potential of this electrogenic exchanger is exceeded during a step increase
in [Ca2+]o even at the transmembrane potential of resting muscle.
