Na+i, K+i and Cl-i regulation of exocytosis in guinea-pig antral mucous cells.
10.3346/jkms.2000.15.S.S36
- Author:
Takashi NAKAHARI
1
;
Shoko FUJIWARA
;
Chikao SHIMAMOTO
Author Information
1. Department of Physiology, Osaka Medical College, Takatsuki, Japan. takan@art.osaka-med.ac.jp
- Publication Type:Research Support, Non-U.S. Gov't
- Keywords:
Gastric Mucin;
Acetylcholine;
Nystatin;
Pertussis Toxin;
G Protein
- MeSH:
Acetylcholine/pharmacology;
Animal;
Cell Membrane Permeability/drug effects;
Exocytosis/physiology*;
Exocytosis/drug effects;
Gastric Mucosa/metabolism;
Gastric Mucosa/cytology;
Guinea Pigs;
Hypertonic Solutions/pharmacology;
Ionophores/pharmacology;
Nystatin/pharmacology;
Pertussis Toxins/pharmacology;
Potassium/pharmacokinetics*;
Pyloric Antrum/metabolism*;
Pyloric Antrum/cytology;
Sodium Chloride/pharmacokinetics*;
Vasodilator Agents/pharmacology
- From:Journal of Korean Medical Science
2000;15(Suppl):S36-S37
- CountryRepublic of Korea
- Language:English
-
Abstract:
Effects of intracellular Na+, K+ and Cl- on Ca(2+)-regulated exocytosis activated by 10 microM acetylcholine (ACh) were studied in guinea-pig antral mucous cells which are permeabilized by nystatin treatment. Ca(2+)-regulated exocytotic events were modulated by [Na+]i, [K+]i and [Cl-]i via mediation of PTX-sensitive G proteins. Increases in [Na+]i and PTX inhibit G protein (G(Na)), which suppressed the exocytosis. Increases in [K+]i caused the exchange of G proteins (from G(Na) to G(K)) to increase, and GK evoked activation of the exocytosis and was inhibited by PTX. Increases in [Cl-]i and PTX inhibit G protein (G(Cl)), which stimulates exocytotic events. Based on these observations, the exocytosis in antral mucous cells were modulated by intracellular ions, concentration of which were increased or decreased by cell volume changes caused by Ach.
