title: Potentiation of nicotinic currents by bradykinin in the paratracheal ganglia neurons of rats.
abstract: The effects of bradykinin on nicotine-induced responses were investigated in neurons dissociated from rat paratracheal ganglia using the nystatin-perforated patch-clamp recording technique. When bradykinin (10(-9) to 10(-8) M) was pretreated and then simultaneously applied with 10(-5) M nicotine, bradykinin potentiated the nicotine-induced currents. The potentiation was mimicked by [Hyp3]-bradykinin and inhibited by HOE-140, pertussis toxin, neomycin and U-73122, but not U-73433. These results suggest that bradykinin potentiates nicotinic currents via bradykinin B2 receptor, pertussis toxin-sensitive G-protein and phospholipase C. Since bradykinin inhibits the M-current via bradykinin B2 receptor and pertussis toxin-insensitive G-protein [Mochidome, T., Ishibashi, H., Takahama, K., 2001. Bradykinin activates airway parasympathetic ganglion neurons by inhibiting M-currents. Neuroscience 105, 785-791.], it seemed that bradykinin B2 receptor activated two distinct signal transduction pathways in the paratracheal ganglia neurons. This effect of bradykinin might cause enhanced synaptic transmission in paratracheal ganglia neurons and contribute to the aggravation of pathological conditions of the lower airway via enhanced acetylcholine release from the postganglionic nerve terminals.
authors.affiliation: Department of Environmental and Molecular Health Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, 5-1 Oe-Honmachi, Kumamoto 862-0973, Japan.
authors.forename: Jian
authors.initials: J
authors.lastname: Rong Zhou
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Shirasaki
authors.forename: Fumio
authors.initials: F
authors.lastname: Soeda
authors.forename: Kazuo
authors.initials: K
authors.lastname: Takahama
mesh_terms: D000818:Animals; D001920:Bradykinin / Q000031:analogs & derivatives / Q000494:pharmacology*; D065094:Bradykinin B2 Receptor Antagonists; D004357:Drug Synergism; D004963:Estrenes / Q000494:pharmacology; D019204:GTP-Binding Proteins / Q000378:metabolism; D005726:Ganglia, Parasympathetic / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D005731:Ganglionic Stimulants / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D009538:Nicotine / Q000494:pharmacology*; D018408:Patch-Clamp Techniques / Q000379:methods; D037342:Pertussis Toxin / Q000494:pharmacology; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D011760:Pyrrolidinones / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D043782:Receptor, Bradykinin B2 / Q000819:agonists / Q000502:physiology; D010738:Type C Phospholipases / Q000037:antagonists & inhibitors / Q000378:metabolism; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D065094:Bradykinin B2 Receptor Antagonists; D004963:Estrenes; D005731:Ganglionic Stimulants; D010726:Phosphodiesterase Inhibitors; D011760:Pyrrolidinones; D043782:Receptor, Bradykinin B2; D014665:Vasodilator Agents; C060229:1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione; D009538:Nicotine; C065679:icatibant; D037342:Pertussis Toxin; D010738:Type C Phospholipases; D019204:GTP-Binding Proteins; D001920:Bradykinin