Abstract

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/m 3) 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 ( B max) of [ 3H]QNB by 40%, without any changes in the dissociation constant ( K d).

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