Regulation of Liver Plasma Membrane Ca2+ Pump
In mammalian tissues, Na2+/Ca2+ exchange and ATP-dependent Ca2+ pump supported by a (Ca2+-Mg2+)ATPase, both located in the plasma membranes, are the two mechanisms responsible for extrusion of Ca2+ out of the cell against its electrochemical gradient (for a review, see ref. 1). The extracellular free Ca2+ concentration is about 104 times that of intracellular free Ca2+ (50–200 nM). Therefore, the maintenance of a low intracellular free Ca2+ level is critical to preserve the integrity of the cell and its responsiveness to multiple external stimuli. It is now well established that a wide variety of hormones and neurotransmitters exert their effects by mobilizing Ca2+ from intracellular stores, namely endoplasmic reticulum1. The resulting increase in free cytosolic Ca2+ is supposed to be the signal which initiates cellular responses1. However, considering the limited capacity of intracellular stores and the maintenance of elevated Ca2+ after the stimulus, one may assume that inhibition of the liver Ca2+ pump by Ca2+ mobilizing hormones explain the prolonged physiological responses. The purpose of the present report is to make the point on our recent results concerning the liver plasma membrane Ca2+ pump and its regulation.
KeywordsATPase Activity Adenylate Cyclase Cholera Toxin Phospholipid Vesicle Liver Plasma Membrane
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