TY - JOUR
T1 - Calcium uptake by intracellular compartments in permeabilised enterocytes effect of inositol 1,4,5 trisphosphate
AU - Velasco, Gloria
AU - Shears, Stephen B.
AU - Michell, Robert H.
AU - Lazo, Pedro S.
PY - 1986/9/16
Y1 - 1986/9/16
N2 - 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 μM) and high ( 12 μM) 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 dibutryl 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.
AB - 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 μM) and high ( 12 μM) 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 dibutryl 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.
UR - http://www.scopus.com/inward/record.url?scp=0022451645&partnerID=8YFLogxK
U2 - 10.1016/S0006-291X(86)80034-1
DO - 10.1016/S0006-291X(86)80034-1
M3 - Article
C2 - 3021134
AN - SCOPUS:0022451645
SN - 0006-291X
VL - 139
SP - 612
EP - 618
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 2
ER -