Abstract
Under physiological conditions the intracellular calcium ion activity is regulated at a level several orders of magnitude lower than that of the extracellular space. However, under the conditions of energy failure the cytosolic Ca2+ concentration increases markedly. The reasons for this are the opening of the voltage-dependent calcium channels within the plasma membrane, the release of Ca2+ from the ATP-dependent sites of sequestration in the endoplasmatic reticulum and the impaired ability of mitochondria to accumulate calcium. The resulting increase in free cytosolic calcium activity disrupts a variety of cellular functions and, in particular, may be responsible in part for the breakdown of membrane phospholipids.
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© 1986 Plenum Press, New York
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Krieglstein, J., Weber, J. (1986). Calcium Entry Blockers Protect Brain Energy Metabolism Against Ischemic Damage. In: Longmuir, I.S. (eds) Oxygen Transport to Tissue VIII. Advances in Experimental Medicine and Biology, vol 200. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5188-7_31
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DOI: https://doi.org/10.1007/978-1-4684-5188-7_31
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