[Mechanism of activation of receptor-operated calcium entry in non-excitable cells].
Inositol phosphates have an important role in Ca2+ mobilization and especially inositol 1, 4, 5-trisphosphate (IP3) is now believed to release Ca2+ from the endoplasmic reticulum (ER). On the other hand, the mechanism of activation of Ca2+ entry is unknown. Non-excitable cells have only receptor-operated Ca2+ channels, lacking voltage-operated Ca2+ channels, and are a useful system for studying signal transduction. In this review, some mechanisms for the regulation of Ca2+ entry in non-excitable cells are discussed and a new hypothesis originally proposed by Putney (1986), the capacitative Ca2+ entry model, is focussed. In this model, Ca2+ influx across the plasma membrane is increased when the IP3-sensitive Ca2+ pools is emptied. Capacitative Ca2+ entry is now confirmed in rat parotid acinar cells by studies on the refilling process for intracellular Ca2+ pools and by using the microsomal Ca(2+)-ATPase inhibitor thapsigargin, which does not increase cellular IP3. Finally, capacitative Ca2+ entry is expected to exist in a variety of cell types including excitable cells.
Takemura
H
H
Department of Pharmacology, Sapporo Medical College, Japan.
Ohshika
H
H
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors; D004721:Endoplasmic Reticulum / Q000378:metabolism; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism / Q000502:physiology*; D015398:Signal Transduction; D013729:Terpenes / Q000494:pharmacology; D019284:Thapsigargin
D015220:Calcium Channels; D013729:Terpenes; D019284:Thapsigargin; D015544:Inositol 1,4,5-Trisphosphate; D000252:Calcium-Transporting ATPases; D002118:Calcium