Abstract

We used autonomic-blocking drugs to define nonadrenergic noncholinergic (NANC) vagus nerve pathways regulating tracheal mucus secretion. In anesthetized cats, mucus glycoconjugates, radiolabeled biosynthetically with [35S]sulfate and [3H]glucose, were washed from a tracheal segment in situ and dialyzed before scintillation counting and chemical assay with periodic acid-Schiff (PAS). Without autonomic blockade, vagal stimulation (9.5 Hz, 10 V, 2-ms pulse width, 10-min duration) increased outputs of radiolabeled and PAS-reactive glycoconjugates repeatably over four stimulation periods. In other animals, vagus nerves were stimulated with administration of autonomic blockers between stimulations. The first stimulation (no blockers) increased glycoconjugate output (delta 35S = 221 +/- 43.3%, delta 3H = 58 +/- 13.8%; delta PAS = +299 +/- 82.7%). Atropine, phentolamine, and propranolol reduced these responses (delta 35S = 67 +/- 15.6%; delta 3H = 26 +/- 5.3%; delta PAS = 88 +/- 25.6%). Guanethidine did not significantly lessen them further, although delta 3H was no longer significant. Ganglion blockade with hexamethonium prevented most of the remaining response to vagal stimulation (P less than 0.05 for diminution of delta 35S and delta PAS), but small effects persisted (delta 35S = 17 +/- 5.6%; delta PAS = 20 +/- 6.8%; P less than 0.05). We conclude that the main NANC vagal pathway controlling tracheal glycoconjugate secretion runs orthodromically.

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