Gmaj P, Murer H
Institute of Physiology, University of Zürich-Irchel, Switzerland.
Miner Electrolyte Metab. 1988;14(1):22-30.
The data which we have reviewed suggest that, at steady state, the cytosolic [Ca2+] is determined by the balance between Ca2+ influx across both the brush border and the basolateral membrane, and Ca2+ extrusion through the basolateral membrane catalyzed predominantly by the calmodulin-activated Ca2+ ATPase. Na+-Ca2+ exchange does not appear to play an important quantitative role in calcium extrusion but may participate in the regulation of cytosolic calcium as a function of luminal sodium entry. Ca2+ transport systems in endomembranes are probably activated only during Ca2+ transients in the cell. Thus, the reticular high-affinity Ca2+ ATPase allows for accumulation of limited amounts of Ca2+ into the reticulum at normal cytosolic Ca2+ concentrations of 0.1-0.2 M; Ca2+ can be rapidly released from this pool by IP3 produced in response to hormonal stimulation, which results in a transient increase in cytosolic Ca2+ and stimulation of calmodulin-dependent enzymes. When Ca2+ entry is stimulated to levels which exceed the capacity of Ca2+ ATPase in the basolateral membrane, cytosolic [Ca2+] may rise above the mitochondrial set point and mitochondrial Ca2+ accumulation may occur. It remains to be investigated if the latter reaction occurs under physiological or only under pathological conditions.
