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(Circulation Research. 2006;99:109.)
© 2006 American Heart Association, Inc.

Editorials

Mitochondrial Buffering of Calcium in the Heart

Potential Mechanism for Linking Cyclic Energetic Cost With Energy Supply?

Patrick G. Sullivan, C. William Balke, Karyn A. Esser

From the Spinal Cord & Brain Injury Research Center (P.G.S.) and the Departments of Anatomy & Neurobiology (P.G.S.), Medicine (C.W.B.), and Physiology (C.W.B., K.A.E.), University of Kentucky College of Medicine, Lexington.

Correspondence to C. William Balke, University of Kentucky, College of Medicine, MN150, Chandler Medical Center, 800 Rose Street, Lexington Kentucky 40536-0298. E-mail b.balke@uky.edu

See related article, pages 172–182

Key Words: heart • mitochondria • calcium buffering

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The kinetics of mitochondrial Ca²⁺ cycling and its precise role in controlling local Ca²⁺ fluxes in intact cardiac myocytes has not been fully elucidated. In the case of cardiac excitation–contraction (E-C) coupling in normal cardiac atrial cells, it has been established that cytosolic Ca²⁺ ([Ca²⁺]_c) increases peripherally within the cell and propagates to the center.¹ What is less clear has been the understanding of the time scale dynamics of the Ca²⁺ fluxes within the mitochondria. To began to address whether beat-to-beat changes in [Ca²⁺]_c alter mitochondrial Ca²⁺ loading, Maack and colleagues² use a novel technique to monitor, simultaneously, Ca²⁺ concentrations in the cytoplasm and mitochondrial matrix. Additionally, the authors’ probe the effect that mitochondrial Ca²⁺ efflux, due to elevated Na⁺, could have on mitochondrial Ca²⁺ buffering and bioenergetics. It is well recognized that the energetic cost of mechanical/contractile work plus ion handling associated with E-C coupling is very high and is supported by the large mitochondrial volume fraction of the cardiac myocyte. The link between regulation of ATP production and intracellular calcium fluxes has been suggested by studies that have demonstrated that the transport of Ca²⁺ into the mitochondrial matrix can activate several enzymes of the TCA cycle.

It is well-known that mitochondria sequester Ca²⁺ ([Ca²⁺]_m) under conditions that increase [Ca²⁺]_c concentrations in many different cell types.^3–5 Changes in [Ca²⁺]_m can have effects on energy production rates, amplitude, and temporal profiles of [Ca²⁺]_c as well as its well described role in . . . [Full Text of this Article]

Related Article:

Elevated Cytosolic Na⁺ Decreases Mitochondrial Ca²⁺ Uptake During Excitation-Contraction Coupling and Impairs Energetic Adaptation in Cardiac Myocytes

Christoph Maack, Sonia Cortassa, Miguel A. Aon, Anand N. Ganesan, Ting Liu, and Brian O’Rourke
Circ. Res. 2006 99: 172-182. [Abstract] [Full Text] [PDF]