Sympathetic nerve disturbance and fine structure of adrenergic nerve terminals in nasal mucosa after experimentally-induced nasal hypersensitivity.
Electron microscopic observations were used to study the relation between the adrenergic nerve terminal and the effector cell in the nasal mucosa of toluene diisocyanate-sensitized and non-sensitized guinea pigs. Adrenergic nerve terminals were abundantly distributed in the adventitia of arterioles, however, no synapse formation was observed in smooth muscle cells of the mesothelium, i.e., effector cells. Adrenergic nerve terminals were observed separated from smooth muscle cells of the mesothelium of the arteriole by distances of 1000 A-3000 A. Neurotransmission by the sympathetic nerve in the nasal mucosa is assumed to be by diffusion of norepinephrine (NE) or by diffusive synaptic conduction. The mechanism of sympathetic hypofunction in the nasal mucosa in nasal hypersensitivity is assumed to be as follows: Released histamine directly stimulates H-1 receptors at the sympathetic nerve terminal, leading to the release of NE. Once released, NE is not readily reabsorbed, and is gradually depleted in the sympathetic nerve terminal, leading to hypofunction of the sympathetic nerve.
Kitajiri
M
M
Department of Otolaryngology, Kansai Medical University, Osaka, Japan.
Kubo
N
N
Tomoda
K
K
Maeda
N
N
Yamashita
T
T
Kumazawa
T
T
D000320:Adrenergic Fibers / Q000502:physiology / Q000648:ultrastructure*; D000818:Animals; D005260:Female; D006168:Guinea Pigs; D008854:Microscopy, Electron; D009297:Nasal Mucosa / Q000294:innervation*; D009411:Nerve Endings / Q000503:physiopathology / Q000648:ultrastructure*; D009638:Norepinephrine / Q000502:physiology; D012130:Respiratory Hypersensitivity / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology; D009435:Synaptic Transmission / Q000502:physiology; D014051:Toluene 2,4-Diisocyanate
D014051:Toluene 2,4-Diisocyanate; D009638:Norepinephrine