Dysfunction of nonadrenergic noncholinergic inhibitory system after antigen inhalation in actively sensitized cat airways

M. Miura, M. Ichinose, K. Kimura, U. Katsumata, T. Takahashi, H. Inoue, T. Takishima

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27 Citations (Scopus)


We have investigated whether proteases released during antigen inhalation cause dysfunction of the nonadrenergic noncholinergic inhibitory nervous system (NANCIS). Frequency-response (F-R) studies of NANCIS were performed before and after Ascaris antigen (ASC) inhalation using actively sensitized cats. NANC dilatatory effects were obtained by stimulating bilateral cervical vagi under cholinergic and β-adrenergic blockade and serotonin-induced bronchoconstriction, and assessed by maximal percent relaxation (r(max)) and the frequency causing 50% of maximal relaxation (EF50). ASC inhalation caused a transient increase in pulmonary resistance in all animals. One hour after ASC inhalation, pulmonary resistance returned to the baseline value, but ASC inhalation significantly attenuated NANC inhibitory activities: r(max) decreased from 82.2 ± 4.7 (mean ± SE) to 64.3 ± 11.2% (p < 0.05), and the geometric mean of EF50 increased from 1.7 to 4.3 Hz (p < 0.05). Dilatatory effects of infused VIP, a possible neurotransmitter of NANCIS, was also attenuated after ASC inhalation. Pretreatment with leupeptin (3 mg/kg) abolished ASC-induced impairment of NANC inhibitory activities. By contrast, dilatatory effects of adrenergic nerve stimulation were not affected by ASC inhalation. These results suggest that NANC inhibitory activities can be impaired after ASC inhalation, and that this impairment of NANCIS may be due to effects of proteases released during allergic reaction.

Original languageEnglish
Pages (from-to)70-74
Number of pages5
JournalAmerican Review of Respiratory Disease
Issue number1
Publication statusPublished - 1992

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine


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