Possible sensory receptor of nonadrenergic inhibitory nervous system

M. Ichinose, H. Inoue, M. Miura, N. Yafuso, H. Nogami, T. Takishima

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9 Citations (Scopus)


To determine the sensory receptor of the nonadrenergic inhibitory nervous system (NAIS), 22 cats were anesthetized and serotonin was continuously administered (50-250 μg·kg-1·min-1 iv) to increase pulmonary resistance (RL) to 377 ± 57% (SE) of the control value. We then 1) mechanically irritated the trachea, 2) intravenously administered capsaicin (5 μg/kg), or 3) induced hypoxia (arterial PO2 30-40 Torr) to stimulate irritant and bronchial C-fiber receptors, pulmonary C-fiber receptors, or the carotid body (chemoreceptors), respectively. After treatment with atropine (3 mg/kg iv) and propranolol (2 mg/kg iv), the serotonin-induced change in RL was reduced by 58.6 ± 14.3% by mechanical irritation and 63.3 ± 12.1% by intravenous capsaicin. However, hypoxia produced no dilatation of the airways. In further experiments, we employed capsaicin inhalation to stimulate bronchial C-fiber receptors. Inhaled capsaicin (0.1%, for 5 breaths) also reduced RL by 79.2 ± 9.2% of the elevated value, after atropine and propranolol. Treatment with a ganglionic blocking agent, hexamethonium (2 mg/kg iv), abolished bronchodilator responses, implying that a reflex pathway through vagal nerves is involved in this phenomenon. These results suggest that pulmonary and bronchial C-fiber receptors may be involved as sensory receptors in NAIS reflex bronchodilatation.

Original languageEnglish
Pages (from-to)923-929
Number of pages7
JournalJournal of Applied Physiology
Issue number3
Publication statusPublished - 1987

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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