Role of nitric oxide released from iNANC neurons in airway responsiveness in cats

H. Aizawa, S. Takata, H. Inoue, Koichiro Matsumoto, H. Koto, N. Hara

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

The precise role of inhibitory nonadrenergic noncholinergic (iNANC) neurons and nitric oxide in airway hyperresponsiveness remains uncertain. The role of NO in the regulation of airway responsiveness was studied in anaesthetized and mechanically ventilated cats. To assess airway responsiveness, the changes in total pulmonary resistance (R(L)) produced by delivering serotonin aerosol to the airways were measured before and after N(ω)-nitro-L-arginine methyl ester (L-NAME), or a ganglionic blocker, hexamethonium, which has been reported to block iNANC. Serotonin was chosen because it causes bronchoconstriction in part by neural reflex. To further clarify the mechanism(s) involved, the effect of inhaled capsaicin was also determined in animals with sustained bronchoconstriction induced by serotonin after treatment with atropine and propranolol. Inhibition of NO synthase by L-NAME or blockade of iNANC neurons by hexamethonium significantly increased airway responsiveness. However, addition of L-NAME did not further increase airway responsiveness in animals treated with hexamethonium. In the presence of atropine and propranolol, inhaled capsaicin caused a marked bronchodilation during serotonin-induced sustained bronchoconstriction. The bronchodilation induced by capsaicin was significantly suppressed by hexamethonium and by L-NAME. These results suggest that the nitric oxide released from inhibitory nonadrenergic noncholinergic neurons is important in modulating the airway responsiveness of cats in vivo.

Original languageEnglish
Pages (from-to)775-780
Number of pages6
JournalEuropean Respiratory Journal
Volume13
Issue number4
DOIs
Publication statusPublished - May 29 1999

Fingerprint

Hexamethonium
NG-Nitroarginine Methyl Ester
Bronchoconstriction
Capsaicin
Serotonin
Nitric Oxide
Cats
Neurons
Atropine
Propranolol
Ganglionic Blockers
Aerosols
Nitric Oxide Synthase
Reflex
Lung
Therapeutics

All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine

Cite this

Role of nitric oxide released from iNANC neurons in airway responsiveness in cats. / Aizawa, H.; Takata, S.; Inoue, H.; Matsumoto, Koichiro; Koto, H.; Hara, N.

In: European Respiratory Journal, Vol. 13, No. 4, 29.05.1999, p. 775-780.

Research output: Contribution to journalArticle

Aizawa, H. ; Takata, S. ; Inoue, H. ; Matsumoto, Koichiro ; Koto, H. ; Hara, N. / Role of nitric oxide released from iNANC neurons in airway responsiveness in cats. In: European Respiratory Journal. 1999 ; Vol. 13, No. 4. pp. 775-780.
@article{03bfdb71af5b4193b2737fe8662358e6,
title = "Role of nitric oxide released from iNANC neurons in airway responsiveness in cats",
abstract = "The precise role of inhibitory nonadrenergic noncholinergic (iNANC) neurons and nitric oxide in airway hyperresponsiveness remains uncertain. The role of NO in the regulation of airway responsiveness was studied in anaesthetized and mechanically ventilated cats. To assess airway responsiveness, the changes in total pulmonary resistance (R(L)) produced by delivering serotonin aerosol to the airways were measured before and after N(ω)-nitro-L-arginine methyl ester (L-NAME), or a ganglionic blocker, hexamethonium, which has been reported to block iNANC. Serotonin was chosen because it causes bronchoconstriction in part by neural reflex. To further clarify the mechanism(s) involved, the effect of inhaled capsaicin was also determined in animals with sustained bronchoconstriction induced by serotonin after treatment with atropine and propranolol. Inhibition of NO synthase by L-NAME or blockade of iNANC neurons by hexamethonium significantly increased airway responsiveness. However, addition of L-NAME did not further increase airway responsiveness in animals treated with hexamethonium. In the presence of atropine and propranolol, inhaled capsaicin caused a marked bronchodilation during serotonin-induced sustained bronchoconstriction. The bronchodilation induced by capsaicin was significantly suppressed by hexamethonium and by L-NAME. These results suggest that the nitric oxide released from inhibitory nonadrenergic noncholinergic neurons is important in modulating the airway responsiveness of cats in vivo.",
author = "H. Aizawa and S. Takata and H. Inoue and Koichiro Matsumoto and H. Koto and N. Hara",
year = "1999",
month = "5",
day = "29",
doi = "10.1034/j.1399-3003.1999.13d13.x",
language = "English",
volume = "13",
pages = "775--780",
journal = "European Respiratory Journal",
issn = "0903-1936",
publisher = "European Respiratory Society",
number = "4",

}

TY - JOUR

T1 - Role of nitric oxide released from iNANC neurons in airway responsiveness in cats

AU - Aizawa, H.

AU - Takata, S.

AU - Inoue, H.

AU - Matsumoto, Koichiro

AU - Koto, H.

AU - Hara, N.

PY - 1999/5/29

Y1 - 1999/5/29

N2 - The precise role of inhibitory nonadrenergic noncholinergic (iNANC) neurons and nitric oxide in airway hyperresponsiveness remains uncertain. The role of NO in the regulation of airway responsiveness was studied in anaesthetized and mechanically ventilated cats. To assess airway responsiveness, the changes in total pulmonary resistance (R(L)) produced by delivering serotonin aerosol to the airways were measured before and after N(ω)-nitro-L-arginine methyl ester (L-NAME), or a ganglionic blocker, hexamethonium, which has been reported to block iNANC. Serotonin was chosen because it causes bronchoconstriction in part by neural reflex. To further clarify the mechanism(s) involved, the effect of inhaled capsaicin was also determined in animals with sustained bronchoconstriction induced by serotonin after treatment with atropine and propranolol. Inhibition of NO synthase by L-NAME or blockade of iNANC neurons by hexamethonium significantly increased airway responsiveness. However, addition of L-NAME did not further increase airway responsiveness in animals treated with hexamethonium. In the presence of atropine and propranolol, inhaled capsaicin caused a marked bronchodilation during serotonin-induced sustained bronchoconstriction. The bronchodilation induced by capsaicin was significantly suppressed by hexamethonium and by L-NAME. These results suggest that the nitric oxide released from inhibitory nonadrenergic noncholinergic neurons is important in modulating the airway responsiveness of cats in vivo.

AB - The precise role of inhibitory nonadrenergic noncholinergic (iNANC) neurons and nitric oxide in airway hyperresponsiveness remains uncertain. The role of NO in the regulation of airway responsiveness was studied in anaesthetized and mechanically ventilated cats. To assess airway responsiveness, the changes in total pulmonary resistance (R(L)) produced by delivering serotonin aerosol to the airways were measured before and after N(ω)-nitro-L-arginine methyl ester (L-NAME), or a ganglionic blocker, hexamethonium, which has been reported to block iNANC. Serotonin was chosen because it causes bronchoconstriction in part by neural reflex. To further clarify the mechanism(s) involved, the effect of inhaled capsaicin was also determined in animals with sustained bronchoconstriction induced by serotonin after treatment with atropine and propranolol. Inhibition of NO synthase by L-NAME or blockade of iNANC neurons by hexamethonium significantly increased airway responsiveness. However, addition of L-NAME did not further increase airway responsiveness in animals treated with hexamethonium. In the presence of atropine and propranolol, inhaled capsaicin caused a marked bronchodilation during serotonin-induced sustained bronchoconstriction. The bronchodilation induced by capsaicin was significantly suppressed by hexamethonium and by L-NAME. These results suggest that the nitric oxide released from inhibitory nonadrenergic noncholinergic neurons is important in modulating the airway responsiveness of cats in vivo.

UR - http://www.scopus.com/inward/record.url?scp=0032958338&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032958338&partnerID=8YFLogxK

U2 - 10.1034/j.1399-3003.1999.13d13.x

DO - 10.1034/j.1399-3003.1999.13d13.x

M3 - Article

C2 - 10362039

AN - SCOPUS:0032958338

VL - 13

SP - 775

EP - 780

JO - European Respiratory Journal

JF - European Respiratory Journal

SN - 0903-1936

IS - 4

ER -