Measurement of Ca2(+)-release-dependent inward current reveals two distinct components of Ca2+ release from sarcoplasmic reticulum in guinea-pig atrial myocytes.
Ca2+ current (L-type) and inward current caused by Ca2+ release from the sarcoplasmic reticulum and carried by electrogenic Na+/Ca2+ exchange have been measured in cultured atrial myocytes from hearts of adult guinea-pigs using whole-cell voltage clamp techniques. The pipette solution, used for internal dialysis of the cells, contained a high concentration, 60 mM or 25 mM, of citrate as a non-saturable low-affinity Ca2(+)-chelating compound. It has been shown previously that Ca2(+)-release-dependent inward current under these conditions is carried by electrogenic Na+/Ca2+ exchange. Furthermore, Ca2(+)-release-dependent inward current (the release signal) can be completely separated from triggering Ca2+ current if brief depolarizations for activating ICa are used. In the majority of cells that did not produce spontaneous Ca2+ release, conditions could be found that caused the release signal to be split into two components: an early component of variable amplitude and a late component of rather constant amplitude. The delay of the late component with regard to triggering ICa was inversely related to the amplitude of the first one. Below a certain amplitude of the first component, the second one failed to be elicited. This suggests the second component to be triggered by the first one. Weakly Ca2(+)-buffered cells produced spontaneous Ca2+ release, resulting in irregular "transient inward currents" at constant membrane-holding potential. Synchronization by trains of step depolarizations unmasked two components also in the spontaneous release signals. In none of the cells studied was any indication of more than two components of the release signal detected. The results are discussed in terms of two distinct compartments of sarcoplasmic reticulum with different properties of Ca2+ release.
Budde
T
T
Department of Cell Physiology, Ruhr-University, Bochum, Federal Republic of Germany.
Lipp
P
P
Pott
L
L
D000818:Animals; D001692:Biological Transport; D002118:Calcium / Q000378:metabolism* / Q000493:pharmacokinetics; D002352:Carrier Proteins / Q000502:physiology; D002462:Cell Membrane / Q000502:physiology; D002478:Cells, Cultured; D004553:Electric Conductivity; D006168:Guinea Pigs; D006325:Heart Atria / Q000166:cytology* / Q000378:metabolism; D008564:Membrane Potentials; D008565:Membrane Proteins / Q000502:physiology; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism / Q000493:pharmacokinetics; D019831:Sodium-Calcium Exchanger
D002352:Carrier Proteins; D008565:Membrane Proteins; D019831:Sodium-Calcium Exchanger; D012964:Sodium; D002118:Calcium