title: Modulation of carbachol-induced Cl(-) currents and fluid secretion by isoproterenol in rat submandibular acinar cells.
abstract: The effects of muscarinic and beta-adrenergic agonists on Cl(-) currents in acinar cells were investigated to clarify their role in the regulation of fluid secretion in rat perfused submandibular glands. Additions of isoproterenol (IPR) at 10(-8) to 10(-6) M and 8-(4-chlorophenylthio)-cyclic AMP (CPT-cAMP) at 10(-3) M to the perfusate suppressed carbachol (CCh; 10(-6) M)-induced fluid secretion. IPR and CPT-cAMP also diminished CCh-induced oscillatory Cl(-) current and increased CCh-stimulated non-oscillatory Cl(-) current. Propranolol blocked the effect of IPR on fluid secretion. IPR did not modulate the CCh-induced increase in intracellular concentration of calcium ions and intracellular pH in isolated cells. Propranolol blocked IPR-induced changes in Cl(- )currents, while propranolol itself increased CCh-induced K(+) current and reduced CCh-induced oscillatory Cl(-) current. Increasing external osmolarity with 50 mM sucrose abolished IPR-enhanced non-oscillatory Cl(-) current. Neither CCh-induced oscillatory Cl(-) current nor IPR-induced suppression of the oscillatory Cl(-) current was influenced by the hypertonicity. Perfusion of the gland with the hypertonic solution did not affect the IPR-induced suppression of fluid secretion. These results suggest that IPR induces the suppression of CCh-induced oscillatory Cl(-) current and potentiation of the non-oscillatory Cl(-) current via an increase in cyclic AMP level, and that suppression of the oscillatory Cl(-) current by IPR may contribute to the inhibition of fluid secretion from submandibular glands.
authors.affiliation: Department of Oral Physiology, Hiroshima University School of Dentistry, Hiroshima, 734-8553, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Tanaka
authors.forename: Y
authors.initials: Y
authors.lastname: Shiba
authors.forename: T
authors.initials: T
authors.lastname: Nakamoto
authors.forename: M
authors.initials: M
authors.lastname: Sugita
authors.forename: C
authors.initials: C
authors.lastname: Hirono
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001826:Body Fluids / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D002217:Carbachol / Q000494:pharmacology*; D002712:Chlorides / Q000502:physiology*; D018679:Cholinergic Agonists / Q000494:pharmacology*; D000242:Cyclic AMP / Q000031:analogs & derivatives / Q000494:pharmacology; D004553:Electric Conductivity; D006863:Hydrogen-Ion Concentration; D006982:Hypertonic Solutions / Q000494:pharmacology; D007477:Ions; D007545:Isoproterenol / Q000494:pharmacology*; D008297:Male; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013363:Submandibular Gland / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D013873:Thionucleotides / Q000494:pharmacology
chemical_list: D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D002712:Chlorides; D018679:Cholinergic Agonists; D006982:Hypertonic Solutions; D007477:Ions; D013873:Thionucleotides; C015929:8-((4-chlorophenyl)thio)cyclic-3',5'-AMP; D002217:Carbachol; D011433:Propranolol; D000242:Cyclic AMP; D007545:Isoproterenol; D002118:Calcium