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KMID : 0376319960080010177
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Dental Journal of CNU
1996 Volume.8 No. 1 p.177 ~ p.188
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Regulation of calcium influx by endogenous nitric oxide in the salivary gland
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Choi Gyeong-Ja
Chung Sung-Su
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Abstract
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Nitric oxide (NO) has been known to function as a cellular signaling messenger in various tissues and organs. The present study was aimed to investigate whether the regulatory mechanisms of calcium influx are mediated by the endogenous NO in submaxillary acinar cells. Effects of agents which stimulate or inhibit the NO-cGMP pathway on the calcium influx and potassium efflux were examined in submaxillary cells of the rat in vitro.
1) In the submandibular slices, carbachol (10^-5 mol/L) increased the NO_2 contents, which was prevented by pretreatment with L-NAME.
2) In the submandibular slices, K^+ efflux in response to carbachol (10^-5 mol/L) was significantly inhibited by pretreatment with L-NAME (10^-4 mol/L) which was attenuated by L-arginine (10^-5 mol/L).
3) L-NAME (10^-4 mol/L) did not affect the transient K^+ efflux in response to carbachol (10^-5 mol/L), but decreased the sustained K^+ efflux.
4) In the isolated submandibular acini, calcium influx by carbachol (10^-5 mol/L) was reduced by L-NAME or L-NMA.
5) In the isolated submandibular acini, calcium influx induced by sodium nitroprusside (10^-6 mol/L) was attenuated by pretreatment with hemoglobin (10^-4 mol/L) or methylene blue (10^-4 mol/L).
6) Calcium influx by 8-Br-cGMP (10^-4 mol/L) was inhibited by H8, (10^-4 mol/L).
7) Calcium influx by 8-Br-cGMP was not affected by nifedipine or verapamil (10^-5 mol/L) but was slightly decreased by reduction of extracellular sodium concentration.
These results suggest that endogenous NO stimulates Ca^2+ influx through activating a cGMP-dependent protein kinase-activated nonselective cation channel in submandibular acinar cells.
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