title: Differences in the Ca2+ response resulting from neurotransmitter stimulations of rat parotid acini and ducts.
abstract: There are few data available regarding the differences in intracellular Ca2+ responses of parotid acinar and ductal cells. This study investigated the Ca2+ mobilization that was induced by the chemical stimulation of acinar and ductal cells from rat parotid glands. In fura-2 loaded parotid cells, carbachol increased the intracellular Ca2+ concentration ([Ca2+](i)) to a greater extent in the acinar cells than in the ductal cells, but noradrenaline increased the [Ca2+](i) in the ductal cells more than in the acinar cells. Although there was no difference in the alpha1-adrenergic receptor agonist phenylephrine-induced Ca2+ mobilization between acini and ducts, the beta-adrenergic receptor agonist isoproterenol increased the [Ca2+](i) in only the ductal cells. Additionally, the effects of non-adrenergic, non-cholinergic neurotransmitters were investigated. Substance P and ATP increased the [Ca2+](i) in parotid acini and/or ducts. A substance P-induced Ca2+ response was observed in only acini, while the ATP-induced Ca2+ response was significantly higher in ducts than in acini. These results suggest that parotid acini have a greater sensitivity to cholinergic and substance P stimulation and a lesser sensitivity to beta-adrenergic and ATP stimulation than the ductal cells. In light of these results, substance P and isoproterenol will be useful for identifying parotid acini and ducts, respectively.
authors.affiliation: Department of Biosciences, Kyushu Dental College, 2-6-1 Manazuru, Kokurakitaku, Kitakyushu, Fukuoka 803-8580, Japan.
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Inagaki
authors.forename: Kentaro
authors.initials: K
authors.lastname: Ono
authors.forename: Wataru
authors.initials: W
authors.lastname: Masuda
authors.forename: Taichi
authors.initials: T
authors.lastname: Iida
authors.forename: Ryuji
authors.initials: R
authors.lastname: Hosokawa
authors.forename: Kiyotoshi
authors.initials: K
authors.lastname: Inenaga
mesh_terms: D000255:Adenosine Triphosphate / Q000494:pharmacology; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology; D018679:Cholinergic Agonists / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D016257:Fura-2 / Q000378:metabolism; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D018377:Neurotransmitter Agents / Q000494:pharmacology*; D010306:Parotid Gland / Q000187:drug effects* / Q000378:metabolism; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013363:Submandibular Gland / Q000187:drug effects* / Q000378:metabolism; D013373:Substance P / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D018679:Cholinergic Agonists; D018377:Neurotransmitter Agents; D010656:Phenylephrine; D013373:Substance P; D000255:Adenosine Triphosphate; D002217:Carbachol; D007545:Isoproterenol; D002118:Calcium; D016257:Fura-2