Acetylcholine release from airway cholinergic nerves in horses with heaves, an airway obstructive disease.
Abstract: The present study was conducted to determine if acetylcholine (ACh) release from airway cholinergic nerves is increased and if modulation of ACh release by prejunctional receptors is altered in horses with heaves, an obstructive airway disease characterized by airway inflammation and bronchospasm. Trachealis strips and bronchial segments of normal horses and horses affected with heaves were suspended in 2-ml tissue baths. ACh release was induced by electrical field stimulation and the bath ACh content was measured by high performance liquid chromatography (HPLC) with electrochemical detection. In response to electrical field stimulation, the rate of ACh release from cholinergic nerves innervating the trachea was not significantly different between the two groups of horses. The nonselective muscarinic receptor antagonist atropine augmented ACh release to the same extent in both groups, indicating that there is no dysfunction of muscarinic autoreceptors on cholinergic nerves of large airways from horses with heaves. Compared with the data from normal horses, the inhibitory effect of the alpha 2-adrenoceptor agonist clonidine on ACh release was lacking in the bronchi and less potent in the trachea, suggesting that the prejunctional alpha 2-adrenoceptors are dysfunctional in horses with heaves. Neither exogenous prostaglandin E2 (PGE2) nor the cyclooxygenase inhibitor indomethacin influenced ACh release from the bronchi, suggesting that a decrease in airway mucosal PGE2 production reported previously in horses with heaves does not alter ACh release.
Publication Date: 1995-03-01 PubMed ID: 7881678DOI: 10.1164/ajrccm/151.3_Pt_1.830Google Scholar: Lookup
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- Journal Article
- Research Support
- U.S. Gov't
- P.H.S.
Summary
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This research studied the release of acetylcholine from airway cholinergic nerves in horses with heaves, an airway obstructive disease, and its regulation by various receptors. The study found no significant difference in acetylcholine release from cholinergic nerves between normal horses and those affected by heaves, but identified that prejunctional alpha 2-adrenoceptors in affected horses are dysfunctional.
Experiment Methods
- The research was conducted on both normal horses and those suffering from heaves, an obstructive airway disease.
- Sections from trachealis strips and bronchial segments of these horses were put into 2-ml tissue baths.
- Acetylcholine release was stimulated using electrical field stimulation and measured with high-performance liquid chromatography (HPLC) having electrochemical detection.
Observations with Respect to Acetylcholine Release
- The rate of stimulated acetylcholine release from cholinergic nerves in the trachea was found to be no different between normal horses and those suffering from the obstructive airway disease.
- The muscarinic receptor antagonist atropine increased acetylcholine release to similar extents in the two groups of horses, indicating no dysfunction of muscarinic autoreceptors in the large airways of horses with heaves.
Prejunctional Alpha 2-Adrenoceptors’ Dysfunction
- An abnormality was observed in terms of the regulation of acetylcholine release through alpha 2-adrenoceptors. Clonidine, an alpha 2-adrenoceptor agonist, had lesser inhibitory influence over acetylcholine release from the bronchi in horses with heaves when compared to normal horses. This suggests a dysfunction of prejunctional alpha 2-adrenoceptors in such horses.
No Influence of Prostaglandin E2 or Indomethacin
- Prostaglandin E2 (PGE2) or the cyclooxygenase inhibitor indomethacin, when added exogenously, showed no effect over acetylcholine release, thereby suggesting that decreased airway mucosal PGE2 production in horses with heaves, as previously reported, does not affect the release of acetylcholine.
Cite This Article
APA
Wang ZW, Yu MF, Robinson NE, Derksen FJ.
(1995).
Acetylcholine release from airway cholinergic nerves in horses with heaves, an airway obstructive disease.
Am J Respir Crit Care Med, 151(3 Pt 1), 830-835.
https://doi.org/10.1164/ajrccm/151.3_Pt_1.830 Publication
Researcher Affiliations
- Pulmonary Laboratory, College of Veterinary Medicine, Michigan State University, East Lansing.
MeSH Terms
- Acetylcholine / metabolism
- Animals
- Atropine / pharmacology
- Bronchi / innervation
- Cholinergic Fibers / metabolism
- Chromatography, High Pressure Liquid
- Clonidine / pharmacology
- Dinoprostone / pharmacology
- Electric Stimulation
- Female
- Horse Diseases / metabolism
- Horses
- Indomethacin / pharmacology
- Lung Diseases, Obstructive / metabolism
- Lung Diseases, Obstructive / veterinary
- Male
- Muscle, Smooth / innervation
- Parasympathetic Nervous System / metabolism
- Receptors, Adrenergic, alpha-2 / physiology
- Receptors, Muscarinic / physiology
- Stimulation, Chemical
- Trachea / innervation
Grant Funding
- HL 49494 / NHLBI NIH HHS
Citations
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