The Regulation of Mitochondrial Calcium Transport in Heart.
Current Topics in Membranes and Transport
This chapter describes the Ca2+ uniporter, the Na+–Ca2+ carrier, the Na+–H+ antiporter, Ca2+ recycling, the kinetic regulation of mitochondrial Ca2+, the effects of catecholamines and glucagon on Ca2+ transport by isolated mitochondria, and the regulation of mitochondrial Ca2+ by catecholamines in vivo. The chapter provides the evidence that Ca2+ cycle indeed operates and examines its steady state behavior, particularly under the influence of hormones that induce a change in mitochondrial Ca2+. Emphasis is placed on the properties and control of the Ca2+ cycle in heart mitochondria. Transport systems of heart mitochondria are characterized, which appear to achieve such a tight regulation by mediating steady-state Ca2+ cycling across the inner membrane. The principal physiological regulators of cardiac muscle contractility are noradrenaline released from sympathetic nerves and circulating catecholamines. The Ca2+ cycle in heart may provide one means of coordinating energy expenditure and oxidative metabolism. While no de-amplification mechanism has been recognized in heart that would depress the relay response to cytosolic Ca2+ during β-adrenergic stimulation, Na+–Ca2+ carrier activation, demonstrated in liver mitochondria, would provide such control, but to date this mechanism has not been demonstrated in heart. © 1985, Elsevier Inc. All rights reserved.
|Title:||The Regulation of Mitochondrial Calcium Transport in Heart|
|UCL classification:||UCL > School of Life and Medical Sciences
UCL > School of Life and Medical Sciences > Faculty of Life Sciences
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