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KMID : 0376319940060010067
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Dental Journal of CNU
1994 Volume.6 No. 1 p.67 ~ p.80
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Role of membrane potential, cell volume, and endogenous nitric oxide for the calcium influx in submandibular acinar cells
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Abstract
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In non-excitable cells, calcium entry pathways have been unknown. Salivary acini are hyprpolarized and cell volume is changed transiently during salivary secretion. The present study was designed to investigate whether membrane potential. cell
volume,
and NO are involved in the regulation of calcium influx in the salivary gland. Effects of changes in membrane potential and cell volume on carbachol and thapsigargin-induced 45Ca2+ uptake and Ca-activated K+ efflux were examined using
submaxillary
acinar cells excised from cats. Effects of L-NAME on carbachol. and thapsigargin-induced 45Ca2+ uptake were also observed.
1) Resting membrane potential of the submaxillary gland was -51.2±5.0mv. Carbachol (10E-5 mol/L) or thapsigargin hyperpolarized acinar cell membrane (-77.3±3.0mV), the degree of which was attenuated by apamin (10E-5 mol/L).
2) Carbachol (10E-5 mol/L)-induced 45Ca2+ uptake and K+ efflux, revealed by the Ca2+ free-Ca2+ reintroduction protocol, were completely blocked by pretreatment of atropine but were partially blocked by its posttreatment.
3) Carbachol (10E-5 mol/L) induced 45Ca2+ uptake and K+ efflux were increased by valinomycin (10E-5 mol/L) as K+ ionophore, and decreased by monensin (10E-5 mol/L), gramicidin(10E-5 mol/L) as Na+ ionophore.
4) Thapsigargin (10E-6 mol/L)-induced 45Ca2+-uptake was diminished by monensin and increased by valinomycin.
5) Carbachol (10E-5 mol/L)-and thapsigargin (10E-6 mol/L)-induced 45Ca2+ uptake was decreased in hypertonic media (attained by addition of 500 mmol/L sucrose) and increased in hypotonic media (0.8×isotonic solution).
6) L-NAME (10E-5 mol/L) increased carbachol (10E-5 mol/L)-induced 45Ca2+ uptake whereas it did not affect thapsigargin-induced 45Ca2+ uptake.
These results suggest that changes in membrane potential and cell volume are involved in the control of Ca2+ influx. The role for endogenous NO in receptor mediated Ca2+ influx in the salivary gland acinar cell is also suggest.
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