Cellular Ca2+ Regulation

This book arose from a meeting held at the University of Washington, Seattle, in July of 1986. The meeting was a satellite symposium of the XXXth International Congress of Physiological Sciences which occurred in Vancouver, canada, at that time. 2 Adjustments in the cytoplasmic Ca + concentration of cells occur in response to a variety of external signals. These fluctuations are a cen tral component of one mechanism by which cells adapt their activities to changes in the external environment and to the requirements of whole body 2 homeostatic mechanisms. It is now clear that redistribution of Ca + within 2 intracellular compartments, as well as changes in the rates of Ca + influx and extrusion at the whole cell level, occur during signal-dependent 2 changes in the cytoplasmic Ca + concentration. In summarizing current research in this area, this volume considers first the properties of indi vidual cation transporting activities located in various cell membranes. It then moves to the cellular level, where the consequence of individual transporting activities acting in concert is examined. l!D.phasis is also 2 p1 aced on pa tho1 ogica1 conditions which resu1 t in loss of cell Ca + regu1 a tion as a part of the disease process. We hope that this approach will help the reader to integrate developments in this large and rapdi1y changing fie1 d.

Inhalt
Mechanism and Regulation of Mitochondrial Ca2+ Transport.- Mechanisms of Mitochondrial Ca2+ Transport.- Permeability Pathways of Ca2+ Efflux from Mitochondria: H+ Specificity and Reversibility of the Permeability Defect.- The Role of Calcium and Phospholipase A2 in Glucagon-Induced Enhancement of Mitochondrial Calcium Retention.- Sodium/Proton Antiporters in the Mitochondrial Inner Membrane.- Monovalent Cation Antiport Reactions in Isolated Mitochondria.- Ca2+ Transport Mechanisms in Microsomes and Membranes.- The Hepatic Microsomal Ca2+ Sequestering System.- Regulation of Liver Plasma Membrane Ca2+ Pump.- Purification of Ca2+-ATPase from Rat Pancreatic Acinar Plasma Membranes Using Calmodulin-Affinity Chromatography (Extended Abstract).- The Relative Importance of Calcium Influx and Efflux Via Na-Ca Exchange in Cultured Myocardial Cells.- Na-Ca Exchange in Cardiac Sarcolemmal Vesicles.- Sodium-Calcium Exchange in Platelet Plasma Membrane Vesicles (Extended Abstract).- Effect of Ca2+ Channel Blockers on Passive Calcium Influx into Re sealed Human Red Blood Cell Ghosts (Extended Abstract).- Pathophysiological Aspects of Ca2+ Transport.- Altered Calcium Homeostasis and Membrane Integrity in Myocardial Cell Injury.- Cellular Ca2+ Dyshomeostasis in the Liver in Endotoxic Shock (Extended Abstract).- Evidence for Hexagonal II Phase Lipid Involvement in Mitochondrial Ca2+ Movements.- Abnormal Ca2+ Transport Characteristics of Hepatoma Mitochondria and Endoplasmic Reticulum.- Alkylating Toxins and the Liver Plasma Membrane Calcium Pump/Calcium ATPase.- Role of ATP and Na+ in the Regulation of Cytosolic Free Calcium in Kidney Cells.- The in Vivo Role of Cellular Ca2+ Pomps in Metabolic Regulation.- Role of Guanine Nucleotide Regulatory Proteins and Inositol Phosphates in the Hormone Induced Mobilization of Hepatocyte Calcium.- Formation and Metabolism of Inositol Phosphates: The Inositol Tris/Tetrakisphosphate Pathway.- Potentiation by GTP of Ins (1,4,5)P3-Induced Ca2+ Mobilization in Permeabilized Hepatocytes (Extended Abstract).- AGEPC: A Potent Calcium-Dependent Chemical Mediator in the Liver.- Role of Local [Ca2+] in the Control of Cell Function.- Calcium and Magnesium Movements Through Sarcoplasmic Reticulum, Endoplasmic Reticulum, and Mitochondria.- Relationship Between Cytosolic Free Calcium Ion Concentration and the Control of Pyruvate Dehydrogenase in Isolated Cardiac Myocytes and Synaptosomes.- The Activation of Pyruvate Dehydrogenase by Glucagon in Hepatocytes Is Diminished by Phorbol Myristate Acetate: A Role for Cytoplasmic Calcium in Dehydrogenase Regulation.- Hormonal Regulation of Intramitochondrial Ca2+ and Oxidative Metabolism in Mammalian Tissues.- Contributors.