title: Calcium uptake by intracellular compartments in permeabilised enterocytes. Effect of inositol 1,4,5 trisphosphate.
abstract: 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.
mesh_terms: 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*
chemical_list: D007295:Inositol Phosphates; D013403:Sugar Phosphates; D015544:Inositol 1,4,5-Trisphosphate; D004492:Edetic Acid; D000242:Cyclic AMP; D011493:Protein Kinase C; D002118:Calcium