The neurogenic responses of tracheal smooth muscles to electrical field stimulation(EFS) is biphasic, consisting firstly of cholinergic contraction followed by a slow and sustained relaxation. It is well known that a sustained relaxation involves
th
inhibitory non-adrenergic systems. This study was done to investigate the relaxing agents and their action mechanisms by use of an organ bath with platiunm.
The tracheal smooth muscle relaxation due to EFS was suppressed by L-NAME, the NO(Nitric Oxide) synthase inhibitor, and these effects were reversed by L-arginine, the precursor of NO. Also, L-NAME(NG-nitro-L-arginine methyl ester) increased the
basal
tension. Nitroprusside, the NO-donor, suppressed the tracheal basal tension greatly. Methylene blue, the inhibitor of guanylate cyclase, decreased EFS-induced relaxations and increased basal tension. Forskolin and isoprenaline, which are
activators
of
adenylate cyclase, suppressed tracheal basal tension in the same way as nitroprusside. TEA(tetraethylammonium), the non-specific K+ channel blocker, and apamin, the Ca2+-activated K+ channel blocker, increased tracheal basal tension and
EFS-induced
relaxations.
Our results indicate that NO is released upon stimulation of the NAN(Non Adrenergic Non Cholinergic)nerves in guinea-pig tracheal smooth muscle and that the release of NO related with the K+channel, as well as the release of other inhibitory
agentsg.)VIP(Vasoactive Intestinal Polypeptide), PHI(Peptide Histidine Isoleusine)> mediated via cAMP(cyclic Adenosine Monophosphate) may be involved in sustained relaxation.
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