In non-excitable cells, calcium entry pathways have been unknown. Salivary acini are hyperpolarized and cell volume is changed transiently during salivary secretion. The present study was designed to investigate whether membrane potential, cell volume...
In non-excitable cells, calcium entry pathways have been unknown. Salivary acini are hyperpolarized 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 ^45Ca^2+ uptake and Ca-activated K^+ efflux were examined using submaxillary acinar cells excised from cats. Effects of L-NAME on carbachol and thapsigargin-induced ^45Ca^2+ uptake were also observed.
1) Resting membrane potential of the submaxillary gland was -51.2 ± 5.0 mV. Carbachol (10^5 mol/L) or thapsigargin hyperpolarized acinar cell membrane (-77.3 ± 3.0 mV), the degree of which was attenuated by apamin (10^+5 mol/L).
2) Carbachol (10^+5 mol/L)-induced ^45Ca^2+ uptake and K^+ efflux, revealed by the Ca^2+ free-Ca^2+ reintroduction protocol, were completely blocked by pretreatment of atropine but were partially blocked by its posttreatment.
3) Carbachol )10^-5 mol/L)-induced ^45Ca^2+ uptake and K^+ efflux were increased by valinomycin (10^-5 mol/L) as K^+ ionophore, and decreased by monensin (10^-5 mol/L), gramicidin (10^5 mol/L) as Na^+ ionophore.
4) Thapsigargin (10^-6 mol/L)-induced ^45Ca^2+ uptake was diminished by monensin and increased by valinomycin.
5) Carbachol (10^-5 mol/L)- and thapsigargin (10^-6 mol/L)-induced ^45Ca^2+ 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 (10^-5 mol/L) increased carbachol (10^-5 mol/L)-induced ^45Ca^2+ uptake whereas it did not affect thapsigargin-induced ^45Ca^2+ uptake.
These results suggest that changes in membrane potential and cell volume are involved in the control of Ca^2+ influx. The role for endogenous NO in regulating receptor mediated Ca^2+ influx in the salivary gland acinar cell is also suggested.