title: Activation of beta-adrenoceptors does not cause any change in cytosolic Ca2+ distribution in rat parotid acinar cells.
abstract: The effects of the beta-adrenoceptor agonist isoproterenol on the distribution of cytosolic Ca2+ concentrations were studied with digital imaging microscopy in fura-2-loaded rat parotid acinar cells. At concentrations < 10 microM, isoproterenol did not cause any measurable change in cytosolic Ca2+ concentration ([Ca2+]i). Monitoring of [Ca2+]i in selected areas of the acinar cells failed to show that stimulation with isoproterenol causes a localized rise in [Ca2+]i at the apical region close to the lumen. As the maximum response of amylase exocytosis is observed at 0.1 or 1 microM isoproterenol [Tanimura, A., Matsumoto, Y., Tojyo, Y., 1990. Evidence that isoproterenol-induced Ca2+-mobilization in rat parotid acinar cells is not mediated by activation of beta-adrenoceptors. Biochim. Biophys. Acta, 1055, pp. 273-277], the data obtained here indicate that the isoproterenol-induced amylase exocytosis is not accompanied by Ca2+ mobilization. The high concentration (100 microM) of isoproterenol caused a small but significant increase in [Ca2+]i, particularly in the apical region. This response was completely attenuated by the alpha-adrenoceptor antagonist phentolamine, but not by the beta-adrenoceptor antagonist propranolol, indicating that the isoproterenol-induced increase in [Ca2+]i resulted from an activation of alpha-adrenoceptors. Further, the effect of cyclic AMP on Ca2+ release from intracellular Ca2+ stores was studied in saponin-permeabilized acinar cells using the lipophilic Ca2+ indicator Calcium Green C18. Cyclic AMP had no effect on the Ca2+ release, while the same acinar cells responded strongly to inositol 1,4,5-trisphosphate. This result does not support the hypothesis that cyclic AMP directly stimulates Ca2+ mobilization in rat parotid acinar cells.
authors.affiliation: Department of Dental Pharmacology, School of Dentistry, Health Sciences University of Hokkaido, Japan. tojyo@hoku-iryo-u.ac.jp
authors.forename: Y
authors.initials: Y
authors.lastname: Tojyo
authors.forename: A
authors.initials: A
authors.lastname: Tanimura
authors.forename: A
authors.initials: A
authors.lastname: Nezu
authors.forename: Y
authors.initials: Y
authors.lastname: Matsumoto
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002463:Cell Membrane Permeability; D000242:Cyclic AMP / Q000494:pharmacology; D003600:Cytosol / Q000378:metabolism; D015544:Inositol 1,4,5-Trisphosphate / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D010306:Parotid Gland / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D010646:Phentolamine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*
chemical_list: D000317:Adrenergic alpha-Antagonists; D000318:Adrenergic beta-Agonists; D011943:Receptors, Adrenergic, beta; D015544:Inositol 1,4,5-Trisphosphate; D000242:Cyclic AMP; D007545:Isoproterenol; D002118:Calcium; D010646:Phentolamine