Receptor-regulated calcium entry.
A wide variety of hormones and neurotransmitters activate cellular responses by mobilizing cellular Ca2+. In general, this Ca2+ mobilization response is comprised of a release of Ca2+ from intracellular stores, as well as increased entry of Ca2+ into the cytoplasm from the extracellular space. The mechanism for release of intracellular Ca2+ results from the Ca2(+)-mobilizing actions of a second messenger, D-myo-inositol 1,4,5-trisphosphate. Inositol polyphosphates appear also to be involved in the activation of Ca2+ entry, but the mechanism by which this is accomplished is less clear. According to the capacitative model for Ca2+ entry, the depletion of the agonist-regulated intracellular Ca2+ pool by the action of D-myo-inositol 1,4,5-trisphosphate is somehow coupled to the activation of Ca2+ entry. The evidence for this model comes from the demonstration, by diverse strategies, that the same Ca2+ entry mechanism normally activated by Ca2(+)-mobilizing agonists can be equally well triggered by depletion of the intracellular Ca2+ pool, even in the absence of receptor activation or elevated cellular levels of inositol polyphosphates.
Putney
J W
JW
Calcium Regulation Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D015544:Inositol 1,4,5-Trisphosphate / Q000494:pharmacology; D018377:Neurotransmitter Agents / Q000494:pharmacology
D002120:Calcium Channel Agonists; D018377:Neurotransmitter Agents; D015544:Inositol 1,4,5-Trisphosphate; D002118:Calcium