Effect of sodium on calcium-dependent force in unstimulated rat cardiac muscle

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)H222-H231
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume15
Issue number2
DOIs
StatePublished - 1984

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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