Origin and modulation of ach release from rat airway cholinergic nerves. Zhu, Feng-Xia, Xiang-Yang Zhang, and N. Edward Robinson. Departments of Large Animal Clinical Sciences and Physiology, Michigan State University, East Lansing, MI 48824-1314
APStracts 3:0151L, 1996.
The release of acetylcholine (ACh) from airway parasympathetic nerves was studied in rat trachea. We established stimulus parameters, examined the role of extracellular calcium, and investigated the origin of the released ACh by use of vesamicol, an inhibitor of ACh uptake into synaptic vesicles. The role of muscarinic autoreceptors and prostanoids on ACh release was also studied. Tracheal rings were incubated in Krebs-Henseleit solution containing neostigmine and guanethidine with or without atropine. ACh release was measured by HPLC with electrochemical detection. ACh release was dependent on frequency (0.5_16 Hz), voltage (10_25 V), and pulse duration (0.5_4 ms). At 4 Hz, one-fifth of electrical field stimulation (EFS)-induced ACh release was extracellular Ca++-independent and vesamicol -resistant, indicating its non-vesicular origin. Three-fifths was Ca++-dependent and vesamicol-sensitive, indicating it was newly synthesized, and one-fifth was Ca++-dependent but vesamicol -resistant, indicating its origin from prestored vesicles. At 16 Hz, two-fifths was non-vesicular and three-fifths was newly synthesized. Blockade of the muscarinic autoreceptor by atropine potentiated the release of ACh four- to fivefold. Neither of the cyclooxygenase inhibitors indomethacin or meclofenamate nor exogenous PGE2 affected ACh release, indicating that inhibitory prostanoids do not modulate ACh release. 

Received 16 January 1996; accepted in final form 23 August 1996.
APS Manuscript Number L18-6.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 September 1996