TY - JOUR
T1 - Effect of sodium on calcium-dependent force in unstimulated rat cardiac muscle
AU - Walford, G. D.
AU - Gerstenblith, G.
AU - Lakatta, E. G.
PY - 1984
Y1 - 1984
N2 - It has previously been demonstrated that 1) changes in superfusate calcium concentration [Ca2+]0 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+]0 is increased from zero to millimolar concentrations, i.e., reperfusion with Ca2+ after 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°C, [Ca2+]0 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+]0) 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+]0. Thus, in unstimulated rat cardiac muscle, Na+(i) modulates the Ca2+ influx resulting from a step increase in [Ca2+]0 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+0 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+]0 even at the transmembrane potential of resting muscle.
AB - It has previously been demonstrated that 1) changes in superfusate calcium concentration [Ca2+]0 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+]0 is increased from zero to millimolar concentrations, i.e., reperfusion with Ca2+ after 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°C, [Ca2+]0 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+]0) 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+]0. Thus, in unstimulated rat cardiac muscle, Na+(i) modulates the Ca2+ influx resulting from a step increase in [Ca2+]0 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+0 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+]0 even at the transmembrane potential of resting muscle.
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U2 - 10.1152/ajpheart.1984.246.2.h222
DO - 10.1152/ajpheart.1984.246.2.h222
M3 - Article
C2 - 6696133
AN - SCOPUS:18844474061
SN - 0363-6135
VL - 15
SP - H222-H231
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 2
ER -