The toxic effect of an AChE-inhibitor on the cholinergic nervous system in airway smooth muscle.
Excessive cholinergic stimulation of presynaptic muscarinic cholinergic receptors, due to complete inhibition of acetylcholinesterase (AChE) by O-(1,2,2-trimethylpropyl)-methyl-phosphonofluoridate (soman), reduced the release of acetylcholine (ACh) from cholinergic nerves in rat bronchi by almost 25%. Furthermore, long-term (40 h) exposure by inhalation of soman (0.45-0.63 mg/m3) reduced the contraction of bronchi induced by ACh by approximately 70%. This is probably due to reduction of the number of muscarinic cholinergic receptors, since there was a reduction in the binding capacity (Bmax) of [3H]QNB by 40%, without any changes in the dissociation constant (Kd).
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Norwegian Defence Research Establishment, Division for Environmental Toxicology, Kjeller, Norway.
D000109:Acetylcholine / Q000378:metabolism*; D000280:Administration, Inhalation; D000818:Animals; D001980:Bronchi / Q000187:drug effects* / Q000201:enzymology / Q000294:innervation; D002799:Cholinergic Fibers / Q000187:drug effects / Q000378:metabolism; D002800:Cholinesterase Inhibitors / Q000633:toxicity*; D002802:Cholinesterases / Q000378:metabolism; D008297:Male; D010275:Parasympathetic Nervous System / Q000187:drug effects*; D011813:Quinuclidinyl Benzilate / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012999:Soman / Q000633:toxicity*; D014316:Tritium
D002800:Cholinesterase Inhibitors; D014316:Tritium; D011813:Quinuclidinyl Benzilate; D012999:Soman; D002802:Cholinesterases; D000109:Acetylcholine