Calcium uptake by intracellular compartments in permeabilised enterocytes. Effect of inositol 1,4,5 trisphosphate.
Treatment of rat small intestine with EDTA produced isolated enterocytes with plasma membranes which were permeable to small ions. When resuspended in a medium designed to resemble the intracellular medium, Ca2+ was accumulated into the cells. Both mitochondrial and a non-mitochondrial (presumably endoplasmic reticulum) compartments were responsible for sequestering the cation, as indicated by the effects of the mitochondrial inhibitors oligomycin and antimycin and of the Ca-ATPase inhibitor sodium orthovanadate assayed at low (0.9 microM) and high (12 microM) free Ca2+ concentrations. Addition of inositol (1,4,5) trisphosphate induced a rapid release of Ca2+ from the non mitochondrial compartment. The effect of inositol trisphosphate was concentration dependent and showed 50% of maximal release at 2 M. Neither cyclic AMP nor dibutyryl cyclic AMP caused release of Ca2+. These findings lend novel support to the possibility that Ca-mediated control of ionic transport in the small intestine is exerted through the phosphatidylinositol-protein kinase C transduction mechanism.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002451:Cell Compartmentation; D002463:Cell Membrane Permeability; D000242:Cyclic AMP / Q000494:pharmacology; D004492:Edetic Acid / Q000494:pharmacology; D004721:Endoplasmic Reticulum / Q000378:metabolism; D015544:Inositol 1,4,5-Trisphosphate; D007295:Inositol Phosphates / Q000494:pharmacology*; D007421:Intestine, Small / Q000166:cytology* / Q000187:drug effects; D008928:Mitochondria / Q000378:metabolism; D011493:Protein Kinase C / Q000378:metabolism; D051381:Rats; D013403:Sugar Phosphates / Q000494:pharmacology*
D007295:Inositol Phosphates; D013403:Sugar Phosphates; D015544:Inositol 1,4,5-Trisphosphate; D004492:Edetic Acid; D000242:Cyclic AMP; D011493:Protein Kinase C; D002118:Calcium