Nitric oxide synthesis causes inositol phosphate production and Ca2+ release in rat parotid acinar cells

2000 ◽  
Vol 440 (2) ◽  
pp. 223-228 ◽  
Author(s):  
K. Tritsaris ◽  
D.K. Looms ◽  
B. Nauntofte ◽  
S. Dissing
Keyword(s):  
Nitric Oxide ◽  
Inositol Phosphate ◽  
Acinar Cells ◽  
Nitric Oxide Synthesis ◽  
Parotid Acinar Cells ◽  
Inositol Phosphate Production ◽  
Rat Parotid

scholarly journals Activation of P2z purinoceptors diminishes the muscarinic cholinergic-induced release of inositol 1,4,5-trisphosphate and stored calcium in rat parotid acini. ATP as a co-transmitter in the stimulus-secretion coupling

1995 ◽  
Vol 312 (2) ◽  
pp. 457-464 ◽  
Author(s):  
T D Jørgensen ◽  
J Gromada ◽  
K Tritsaris ◽  
B Nauntofte ◽  
S Dissing
Keyword(s):  
Phospholipase C ◽  
Inositol Phosphate ◽  
Acinar Cells ◽  
Inhibitory Effect ◽  
Coupled Processes ◽  
Parotid Acinar Cells ◽  
Inositol Phosphate Production ◽  
Dependent Inhibition ◽  
Muscarinic Cholinergic ◽  
Rat Parotid

The effect of extracellular ATP on the intracellular free Ca2+ concentration ([Ca2+]i) and inositol phosphate production following stimulation with the muscarinic cholinergic agonist acetylcholine (ACh) was investigated in isolated rat parotid acinar cells. Stimulation of rat parotid acinar cells with ATP4- results in a rise in [Ca2+]i that is due to influx of extracellular Ca2+ and mobilization of Ca2+ from intracellular stores. Stimulation with purinergic agonists revealed that both influx as well as Ca2+ release from intracellular stores was mediated through activation of P2z receptors. The Ca2+ mobilization from intracellular stores was due to production of Ins(1,4,5)P3 and was inhibited by U73122, an inhibitor of phospholipase C-coupled processes. Under Ca(2+)-free conditions ATP4- caused a dose-dependent inhibition (IC50 = 8 microM) of the ACh-evoked Ca2+ release. The inhibitory effect of ATP4- is due to activation of the P2z purinoceptors, which results in a strong reduction in the ACh-induced inositol phosphate production. Prestimulation with 100 microM ATP4- reduced the amount of Ins(1,4,5)P3 formed after maximal ACh stimulation by 91%. In conclusion, the inhibitory effect of ATP4- on the ACh-mediated response is due to interactions of the activated P2z receptor with the phospholipase C-coupled processes underlying the muscarinic cholinergic response.

Nitric oxide synthesis causes inositol phosphate production and Ca

2000 ◽  
Vol 440 (2) ◽  
pp. 223 ◽  
Author(s):  
K. Tritsaris ◽  
D.K. Looms ◽  
B. Nauntofte ◽  
S. Dissing
Keyword(s):  
Nitric Oxide ◽  
Inositol Phosphate ◽  
Nitric Oxide Synthesis ◽  
Inositol Phosphate Production

scholarly journals Nitric oxide and cGMP activate Ca2+-release processes in rat parotid acinar cells

2001 ◽  
Vol 355 (1) ◽  
pp. 87 ◽  
Author(s):  
Dagnia K. LOOMS ◽  
Katerina TRITSARIS ◽  
Birgitte NAUNTOFTE ◽  
Steen DISSING
Keyword(s):  
Nitric Oxide ◽  
Acinar Cells ◽  
Parotid Acinar Cells ◽  
Rat Parotid ◽  
Release Processes

scholarly journals β-Adrenergic stimulation alters oligosaccharide pyrophosphoryl dolichol metabolism in rat parotid acinar cells

1985 ◽  
Vol 231 (2) ◽  
pp. 431-438 ◽  
Author(s):  
S R Grant ◽  
E E Kousvelari ◽  
D K Banerjee ◽  
B J Baum
Keyword(s):  
Half Life ◽  
Specific Radioactivity ◽  
Acinar Cells ◽  
Protein Glycosylation ◽  
Significant Enhancement ◽  
Adrenergic Stimulation ◽  
Parotid Acinar Cells ◽  
Secretory Glycoproteins ◽  
Rat Parotid ◽  
Stimulation Of

beta-Adrenergic stimulation of rat parotid acinar cells markedly increases [3H]mannose incorporation into N-linked glycoproteins [Kousvelari, Grant, Banerjee, Newby & Baum (1984) Biochem. J. 222, 17-24]. More than 90% of this protein-bound [3H]mannose was preferentially incorporated into four secretory glycoproteins. The ratio of [3H]mannose/[14C]leucine present in these individual proteins was 1.7-4-fold greater with isoproterenol-treated cells than with untreated controls. In isoproterenol-stimulated cells, [3H]mannose incorporation into mannosylphosphoryl dolichol and oligosaccharide-PP-dolichol was increased 2-3-fold over that observed in unstimulated cells. Similarly, formation of mannosylated oligosaccharide-PP-dolichol was increased approx. 4-fold in microsomes prepared from isoproterenol-treated cells. Also, turnover of oligosaccharide-PP-dolichol was significantly increased (5-fold) by β-adrenergic stimulation; the half-life for oligosaccharide-PP-dolichol decreased from 6 min in control cells to 1.2 min in isoproterenol-stimulated cells. By 15 min after isoproterenol addition to acinar cells, the specific radioactivity of parotid oligosaccharide moieties increased about 3-fold over the value observed in the absence of the agonist. Taken together, these results strongly suggest that elevation of N-linked protein glycosylation in rat parotid acinar cells after β-adrenoreceptor stimulation resulted from significant enhancement in the synthesis of mannosylphosphoryl dolichol and oligosaccharide-PP-dolichol and the turnover of oligosaccharide-PP-dolichol.

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