Intracellular calcium transients evoked by pulsed infrared radiation in neonatal cardiomyocytes
Article first published online: 14 MAR 2011
© 2011 The Authors. Journal compilation © 2011 The Physiological Society
The Journal of Physiology
Volume 589, Issue 6, pages 1295–1306, March 2011
How to Cite
Dittami, G. M., Rajguru, S. M., Lasher, R. A., Hitchcock, R. W. and Rabbitt, R. D. (2011), Intracellular calcium transients evoked by pulsed infrared radiation in neonatal cardiomyocytes. The Journal of Physiology, 589: 1295–1306. doi: 10.1113/jphysiol.2010.198804
- Issue published online: 14 MAR 2011
- Article first published online: 14 MAR 2011
- (Received 30 August 2010; accepted after revision 11 January 2011; first published online 17 January 2011)
Non-technical summary We have investigated the mechanisms underlying the response of cells to pulsed infrared radiation (IR, ∼1862 nm) using the neonatal rat ventricular cardiomyocyte as a model. Fluorescence monitoring of the intracellular free calcium (Ca2+) demonstrated that infrared irradiation induced rapid (millisecond time scale) intracellular Ca2+ transients in the cells. The results showed that the Ca2+ transients were sufficient to elicit contractile responses from the cardiomyocytes and could be ‘paced’ or entrained to the pulsing frequency of the IR. Pharmacological results strongly implicate mitochondria as the primary intracellular organelles contributing to the IR-evoked Ca2+ cycling.
Abstract Neonatal rat ventricular cardiomyocytes were used to investigate mechanisms underlying transient changes in intracellular free Ca2+ concentration ([Ca2+]i) evoked by pulsed infrared radiation (IR, 1862 nm). Fluorescence confocal microscopy revealed IR-evoked [Ca2+]i events with each IR pulse (3–4 ms pulse−1, 9.1–11.6 J cm−2 pulse−1). IR-evoked [Ca2+]i events were distinct from the relatively large spontaneous [Ca2+]i transients, with IR-evoked events exhibiting smaller amplitudes (0.88 ΔF/F0 vs. 1.99 ΔF/F0) and shorter time constants (τ= 0.64 s vs. 1.19 s, respectively). Both IR-evoked [Ca2+]i events and spontaneous [Ca2+]i transients could be entrained by the IR pulse (0.2–1 pulse s−1), provided the IR dose was sufficient and the radiation was applied directly to the cell. Examination of IR-evoked events during peak spontaneous [Ca2+]i periods revealed a rapid drop in [Ca2+]i, often restoring the baseline [Ca2+]i concentration, followed by a transient increase in [Ca2+]i. Cardiomyocytes were challenged with pharmacological agents to examine potential contributors to the IR-evoked [Ca2+]i events. Three compounds proved to be the most potent, reversible inhibitors: (1) CGP-37157 (20 μm, n= 12), an inhibitor of the mitochondrial Na+/Ca2+ exchanger (mNCX), (2) Ruthenium Red (40 μm, n= 13), an inhibitor of the mitochondrial Ca2+ uniporter (mCU), and (3) 2-aminoethoxydiphenylborane (10 μm, n= 6), an IP3 channel antagonist. Ryanodine blocked the spontaneous [Ca2+]i transients but did not alter the IR-evoked events in the same cells. This pharmacological array implicates mitochondria as the major intracellular store of Ca2+ involved in IR-evoked responses reported here. Results support the hypothesis that 1862 nm pulsed IR modulates mitochondrial Ca2+ transport primarily through actions on mCU and mNCX.