Inhibition by L-N(G)-Nitro-L-arginine of nonadrenergic-noncholinergic- mediated relaxations of human isolated central and peripheral airways

J. L. Ellis, B. J. Undem

Research output: Contribution to journalArticle

Abstract

Human isolated central (5 to 12 mm) and peripheral (< 2 mm) bronchi were contracted with 3 μM histamine. Relaxations were then evoked by electrical field stimulation (EFS) (1 to 32 Hz, 1 ms, 12 V for 15 s in the presence of indomethacin, atropine, and propranolol). The magnitude, time-course, and frequency-response relationship of these nonadrenergic, noncholinergic (NANC) relaxations were similar in the central and the peripheral airways. N(G)- Nitro-L-arginine (L-NOARG) (10 μM) inhibited the tetrodotoxin-sensitive NANC relaxations in both central and peripheral bronchi, whereas the stereoisomer D-NOARG was without effect. This inhibition was reversed by L-arginine (1 mM) but not be D-arginine (1 mM). The nitric oxide donor compound, 3- morpholinosydnonimine (SIN-1), was equipotent at relaxing the central and peripheral airways. Vasoactive intestinal peptide (VIP), although it relaxed central airways, was virtually ineffective in relaxing the peripheral airways. In addition, the peptidase, α-chymotrypsin, at a concentration that blocked relaxations to VIP, was without effect on NANC relaxations in the central bronchi. The results support the following hypotheses: (1) both central and peripheral airways receive nonadrenergic relaxant innervation; (2) the relaxant response to electrical stimulation of this system is dependent on a pathway involving L-arginine; and (3) the relaxant response does not appear to involve VIP, but it may involve the production of nitric oxide.

Original languageEnglish (US)
Pages (from-to)1543-1547
Number of pages5
JournalAmerican Review of Respiratory Disease
Volume146
Issue number6
DOIs
StatePublished - 1992

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

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