Cross‐talk between L‐type Ca2+ channels and mitochondria

Abstract

1. Calcium is necessary for myocardial function, including contraction and maintenance of cardiac output. Calcium is also necessary for myocardial energetics and production of ATP by mitochondria, but the mechanisms for calcium regulation by mitochondria are still not fully resolved. 2. The cytoskeleton plays an important role in maintaining a cell's integrity. It is now recognized that cytoskeletal proteins can also assist in the transmission of signals from the plasma membrane to intracellular organelles. Cytoskeletal proteins can regulate the function of the L-type Ca(2+) channel and alter intracellular calcium homeostasis. 3. Recent evidence suggests that calcium influx through the L-type Ca(2+) channel is sufficient to alter a number of mitochondrial functional parameters, including superoxide production, NADH production and metabolic activity, assessed as the formation of formazan from tetrazolium salt. This occurs in a calcium-dependent manner. 4. Activation of the L-type Ca(2+) channel also alters mitochondrial membrane potential in a calcium-independent manner and this is assisted by movement of the auxiliary beta(2)-subunit through F-actin filaments. 5. Because the L-type Ca(2+) channel is the initiator of contraction, a functional coupling between the channels and mitochondria may assist in meeting myocardial energy demand on a beat-to-beat basis.