Increase in Ca2+ Permeability of Intracellular Ca2+ Store Membrane of Saponin-Treated Guinea Pig Peritoneal Macrophages by Inositol 1,4,5-Trisphosphate

Inositol 1,4,5-trisphosphate (InsP3) releases Ca2+ from the non-mitochondrial Ca2+ store site of various types of cells. To study the mechanisms of the Ca2+ release from the store site, the effect of InsP3 on the passive Ca2+ release and influx, and the active Ca2+ uptake in the presence of oxalate,...

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Published in:Journal of biochemistry (Tokyo) 1985-06, Vol.97 (6), p.1575-1582
Main Authors: HIRATA, Masato, KUKITA, Masataka, SASAGURI, Toshiyuki, SUEMATSU, Eiichi, HASHIMOTO, Toshihiko, KOGA, Toshitaka
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - physiology
Animals
Calcium - metabolism
Erythrocytes - metabolism
Guinea Pigs
Humans
In Vitro Techniques
Inositol 1,4,5-Trisphosphate
Inositol Phosphates - pharmacology
Intracellular Membranes - drug effects
Intracellular Membranes - metabolism
Liposomes - metabolism
Macrophages - metabolism
Peritoneal Cavity
Permeability
Saponins - pharmacology
Sugar Phosphates - pharmacology
Vanadates
Vanadium - pharmacology
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Summary:Inositol 1,4,5-trisphosphate (InsP3) releases Ca2+ from the non-mitochondrial Ca2+ store site of various types of cells. To study the mechanisms of the Ca2+ release from the store site, the effect of InsP3 on the passive Ca2+ release and influx, and the active Ca2+ uptake in the presence of oxalate, was examined using saponintreated guinea pig peritoneal macrophages. InsP3 stimulated the passive Ca2+ release and influx. Although InsP3 slightly inhibited the active Ca2+ uptake in the presence of oxalate, it seems unlikely that the Ca2+ release by this agent is caused by the inhibition of the Ca2+ uptake, because the addition of apyrase or hexokinase (which removes ATP within 30 s, so that no more Ca2+ can be accumulated) or vanadate (which inhibits the Ca2+ uptake) resulted in very slow release of Ca2+. These results suggest that the Ca2+ permeability of the Ca2+ store membrane is increased by InsP3. InsP3 did not cause an increase in the Ca2+ permeability of phospholipid vesicles (liposomes), indicating that this agent may bring about Ca2+ release by a specific effect on the physiologically relevant Ca2+ channels or carriers in the non-mitochondrial Ca2+ store site. The passive Ca2+ release by InsP3 was enhanced by ATP and an unhydrolyzable ATP analogue, 5'-adenylyimidodiphosphate, but not by ADP or AMP. The passive Ca2+ release by InsP3 was observed even at 0°C.
ISSN:0021-924X
DOI:10.1093/oxfordjournals.jbchem.a135214