Reconstitution of a passive Ca2+-transport pathway from the basolateral plasma membrane of rat parotid gland acinar cells

1995 ◽  
Vol 148 (3) ◽  
Author(s):  
T. Lockwich ◽  
J. Chauthaiwale ◽  
S.V. Ambudkar ◽  
I.S. Ambudkar
Keyword(s):  
Plasma Membrane ◽  
Parotid Gland ◽  
Acinar Cells ◽  
Transport Pathway ◽  
Rat Parotid Gland ◽  
Basolateral Plasma Membrane ◽  
Rat Parotid

scholarly journals Calcium transport mechanisms in basolateral plasma membrane-enriched vesicles from rat parotid gland

1985 ◽  
Vol 227 (1) ◽  
pp. 239-245 ◽  
Author(s):  
T Takuma ◽  
B L Kuyatt ◽  
B J Baum
Keyword(s):  
Plasma Membrane ◽  
Parotid Gland ◽  
Gradient Centrifugation ◽  
Membrane Vesicles ◽  
Transport Systems ◽  
Transport Mechanisms ◽  
Plasma Membrane Vesicles ◽  
Rat Parotid Gland ◽  
Basolateral Plasma Membrane ◽  
Rat Parotid

Ca2+ transport was studied by using basolateral plasma membrane vesicles from rat parotid gland prepared by a Percoll gradient centrifugation method. In these membrane vesicles, there were two Ca2+ transport systems; Na+/Ca2+ exchange and ATP-dependent Ca2+ transport. An outwardly directed Na+ gradient increased Ca2+ uptake. Ca2+ efflux from Ca2+-preloaded vesicles was stimulated by an inwardly directed Na+ gradient. However, Na+/Ca2+ exchange did not show any ‘uphill’ transport of Ca2+ against its own gradient. ATP-dependent Ca2+ transport exhibited ‘uphill’ transport. An inwardly directed Na+ gradient also decreased Ca2+ accumulation by ATP-dependent Ca2+ uptake. The inhibition of Ca2+ accumulation was proportional to the external Na+ level. Na+/Ca2+ exchange was inhibited by monensin, tetracaine and chlorpromazine, whereas ATP-dependent Ca2+ transport was inhibited by orthovanadate, tetracaine and chlorpromazine. Oligomycin had no effect on either system. These results suggest that in the parotid gland cellular free Ca2+ is extruded mainly by an ATP-dependent Ca2+ transport system, and Na+/Ca2+ exchange may modify the efficacy of that system.

scholarly journals Lithium-induced reduction in intracellular inositol supply in cholinergically stimulated parotid gland

1986 ◽  
Vol 234 (1) ◽  
pp. 199-204 ◽  
Author(s):  
C P Downes ◽  
M A Stone
Keyword(s):  
Parotid Gland ◽  
Acinar Cells ◽  
Phospholipid Metabolism ◽  
Cholinergic Stimulation ◽  
Inositol Phosphatase ◽  
Agonist Stimulation ◽  
Rat Parotid Gland ◽  
Inositol Phospholipid ◽  
Rat Parotid ◽  
Phosphatidylinositol 4

The effects of lithium and cholinergic stimulation on inositol phospholipid metabolism have been assessed using rat parotid gland slices and isolated acinar cells labelled with 32Pi. Cholinergic stimulation using carbachol caused substantial breakdown of phosphatidylinositol 4,5-bisphosphate (PtdInsP2) and enhanced labelling of phosphatidate (PA) and phosphatidylinositol (PtdIns). Lithium alone had little effect upon 32Pi incorporation, but in combination with carbachol it greatly reduced the PtdIns labelling response to the agonist. Instead the label accumulated in a lipid identified as cytidine monophosphorylphosphatidate. There was also an enhancement of the PA labelling response to carbachol. These lithium-induced alterations in agonist-stimulated phospholipid metabolism were reversed if 10-30 mM-inositol was included in the incubation medium. Despite reduced PtdIns synthesis, lithium had relatively little effect on polyphosphoinositide labelling in stimulated cells. Resynthesis of polyphosphoinositides was monitored in acinar cells that had been stimulated with carbachol and then treated with atropine to block muscarinic receptors. Treatment with lithium during the carbachol-stimulation phase reduced the rate of phosphatidylinositol 4-phosphate synthesis, but had no significant effect upon PtdInsP2. The results suggest that an active inositol phosphatase pathway is essential to maintain intracellular inositol levels, but that PtdInsP2 synthesis is not markedly reduced by a substantial fall in intracellular inositol. This implies a close control over the rates of PtdInsP2 breakdown and resynthesis during agonist stimulation.

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