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KMID : 0370220040480060352
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Yakhak Hoeji
2004 Volume.48 No. 6 p.352 ~ p.356
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Regulation of Atrial Ca2+ Signaling by Inositol 1,4,5-Trisphosphate Receptor and Mitochondria
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이향진/Lee HJ
우선희/Lars Cleemann/Martin Morad/Woo SH/Cleemann L/Marad M
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Abstract
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Atrial myocytes have two functionally separate groups of ryanodine receptors (RyRs): those at the periphery colocalized with L-type Ca2+channels (DHPRS) and those at the cell interior not associated with DHPRs. Ca2+ current (1Ca) directly gates peripheral RyRs on action potential and the subsequent peripheral Ca2+ release propagates into the center of atrial myocytes. The mechanisms that regulate the Ca2+ propagation wave remain Poorly understood. Using 2-D confocal Ca2+ imaging, we examined the role of inositol 1,4,5-trisphosphate receptor (IP 3R) and mitochondria on Ica- gated local Ca2+ signaling in rat atrial myocytes. Blockade of IP3R by xestospongin C (XeC) partially suppressed the magnitudes of I ca-gated central and peripheral Ca2+ releases with no effect on Ica-. Mitochondrial staining revealed that mitochondria were aligned with ?2-㎛ separations in the entire cytoplasm of ventricular and atrial myocytes. Membrane depolarization induced rapid mitochondrial Ca2+ rise and decay in the cell periphery with slower rise in the center, suggesting that mitochondria may immediately uptake cytosolic Ca2+, released from the peripheral SR on depolarization, and re-release the Ca 2+ into the cytosol to activate neighboring central RyRs. Our data suggest that the activation of IP 3R and mitochondrial Ca2+ handing on action potential may serve as a cofactor for the Ca2+ propagation from the DHPR-coupled RyRs to the DHPR-uncoupled RyRs with large gaps between them.
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