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Niggli E, Lederer WJ. Activation of Na-Ca exchange current by photolysis of "caged calcium". Biophys J. 1993;65(2):882-91doi: 10.1016/S0006-3495(93)81105-6.
Niggli, E., & Lederer, W. J. (1993). Activation of Na-Ca exchange current by photolysis of "caged calcium". Biophysical journal, 65(2), 882-91. https://doi.org/10.1016/S0006-3495(93)81105-6
Niggli, E, and Lederer, W J. "Activation of Na-Ca exchange current by photolysis of "caged calcium"." Biophysical journal vol. 65,2 (1993): 882-91. doi: https://doi.org/10.1016/S0006-3495(93)81105-6
Niggli E, Lederer WJ. Activation of Na-Ca exchange current by photolysis of "caged calcium". Biophys J. 1993 Aug;65(2):882-91. doi: 10.1016/S0006-3495(93)81105-6. PMID: 8218911; PMCID: PMC1225788.
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Elsevier Science Free PMC Article

Biophys J. 1993 Aug;65(2):882-91. doi: 10.1016/S0006-3495(93)81105-6.

Activation of Na-Ca exchange current by photolysis of "caged calcium".

Biophysical journal

E Niggli, W J Lederer

Affiliations

  1. Department of Physiology, University of Bern, Switzerland.

PMID: 8218911 PMCID: PMC1225788 DOI: 10.1016/S0006-3495(93)81105-6
Free PMC Article

Abstract

Intracellular photorelease of Ca2+ from "caged calcium" (DM-nitrophen) was used to investigate the Ca(2+)-activated currents in ventricular myocytes isolated from guinea pig hearts. The patch-clamp technique was applied in the whole-cell configuration to measure membrane current and to dialyze the cytosol with a pipette solution containing the caged compound. In the presence of inhibitors for Ca2+, K+, and Na+ channels, concentration jumps of [Ca2+]i induced a rapidly activating inward Na-Ca exchange current which then decayed slowly (tau approximately 500 ms). The initial peak of the inward current and the time-course of current decay were voltage-dependent, and no reversal of the current direction was found between -100 and +100 mV. The observed shallow voltage dependence can be described in terms of the movement of an apparently fractional elementary charge (+0.44e-) across an energy barrier located symmetrically in the electrical field of the membrane. The currents were dependent on extracellular Na+ with a half-maximal activation at 73 mM and a Hill coefficient of 2.8. No change of membrane conductance was activated by the Ca2+ concentration jump when extracellular Na+ was completely replaced by Li+ or N-methyl-D-glucamine (NMG) or when the Na-Ca exchange was inhibited by extracellular Ni2+, La3+, or dichlorobenzamil (DCB). The velocity of relengthening after a twitch induced by photorelease of Ca2+ was only reduced drastically when both the sarcoplasmic reticulum and the Na-Ca exchange were inhibited suggesting that all other Ca2+ removing mechanisms have a low transport capacity under these conditions. In conclusion, we have used a novel approach to study Na-Ca exchange activity with photolysis of "caged" calcium. We found that in guinea pig heart muscle cells the Na-Ca exchange is a potent mechanism for Ca2+ extrusion, is weakly voltage-dependent (118 mV for e-fold change) and can be studied without contamination with other Ca(2+)-activated currents.

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