Excitatory prejunctional beta 2-adrenoceptor distribution within equine airway cholinergic nerves.
Abstract: We examined the effect of activation of beta 2-adrenoceptor (AR) by isoproterenol (ISO) on acetylcholine (ACh) release evoked by electrical field stimulation (EFS: 20 V, 0.5 Hz, 0.5 msec) from cholinergic nerves in five regions of equine airways. We also tested if the effect of ISO was dependent on epithelium or prostanoids by examining the effect of ISO on ACh release in the presence and absence of epithelium or cyclooxygenase inhibition. Trachealis strips or bronchial rings were preincubated for 60 min with 10(-7) M atropine, 10(-6) M neostigmine, and 10(-5) M guanethidine. The ACh amount was measured by high-performance liquid chromatography with electrochemical detection. Isoproterenol (10(-8)-10(-6) M) augmented ACh release throughout the whole airway in a concentration-dependent manner. Rubbing off the epithelium potentiated EFS-induced ACh release but neither epithelium removal nor cyclooxygenase inhibition affected the magnitude of ISO-induced augmentation of ACh release. These results indicate that in equine airway parasympathetic nerves: (1) excitatory prejunctional beta 2-adrenoceptors are distributed throughout the tracheobronchial tree; (2) the function of this excitatory beta 2-adrenoceptor is independent of endogenous prostanoids and epithelium; and (3) there is an epithelium-derived factor that inhibits ACh release.
Publication Date: 1996-10-01 PubMed ID: 8946580DOI: 10.1016/0034-5687(96)00062-xGoogle Scholar: Lookup
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- Journal Article
- Research Support
- U.S. Gov't
- P.H.S.
Summary
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The research studied the effect of a specific activator, isoproterenol, on the release of acetylcholine, a critical neurotransmitter, from nerves in different areas of horse’s airways. The study concluded that excitatory prejunctional beta 2-adrenoceptors, which are found all over these nerves, are involved in this process and function without being affected by certain factors including endogenous prostanoids and epithelium.
Objective of the research
- The main goal of this study was to investigate how the activation of beta 2-adrenoceptor by isoproterenol affects the release of acetylcholine, a neurotransmitter, from cholinergic nerves in different regions of equine airways.
- The study also looked into whether this effect of isoproterenol is dependent on the epithelium or prostanoids.
Methodology
- The researchers carried out the study on trachealis strips or bronchial rings which were preincubated with certain medications.
- The amount of acetylcholine released was measured using high-performance liquid chromatography with electrochemical detection.
Results
- The researchers found that isoproterenol augments the release of acetylcholine throughout the airways in a concentration-dependent manner.
- Removal of the epithelium or inhibition of cyclooxygenase didn’t affect the magnitude of how isoproterenol augmented the release of acetylcholine.
Conclusions
- The study concludes that excitatory prejunctional beta 2-adrenoceptors are distributed throughout the pulmonary tree, playing a crucial role in acetylcholine release.
- The functionality of this adrenoceptor doesn’t depend on endogenous prostanoids and epithelium.
- The findings also suggest that a factor derived from the epithelium inhibits the release of acetylcholine.
Cite This Article
APA
Zhang XY, Zhu FX, Robinson NE.
(1996).
Excitatory prejunctional beta 2-adrenoceptor distribution within equine airway cholinergic nerves.
Respir Physiol, 106(1), 81-90.
https://doi.org/10.1016/0034-5687(96)00062-x Publication
Researcher Affiliations
- Department of Large Animal Clinical Sciences, Michigan State University, East Lansing 48824-1314, USA.
MeSH Terms
- Acetylcholine / metabolism
- Adrenergic beta-Agonists / pharmacology
- Animals
- Cholinergic Fibers / drug effects
- Cholinergic Fibers / physiology
- Chromatography, High Pressure Liquid
- Electric Stimulation
- Epithelium / drug effects
- Epithelium / metabolism
- Horses
- Isoproterenol / pharmacology
- Parasympathetic Nervous System / physiology
- Prostaglandins / pharmacology
- Receptors, Adrenergic, beta-2 / drug effects
- Receptors, Adrenergic, beta-2 / metabolism
- Respiratory Physiological Phenomena
- Respiratory System / drug effects
- Respiratory System / innervation
- Signal Transduction / drug effects
- Signal Transduction / physiology
Grant Funding
- HL-49494 / NHLBI NIH HHS
Citations
This article has been cited 1 times.- Nie Z, Fryer AD, Jacoby DB. β2-Agonists inhibit TNF-α-induced ICAM-1 expression in human airway parasympathetic neurons.. PLoS One 2012;7(9):e44780.
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