PGE2 inhibits acetylcholine release from cholinergic nerves in canine but not equine airways.
Abstract: The effects of exogenous prostaglandin E2 (PGE2) and endogenous prostanoids on cholinergic neurotransmission were determined by measurement of acetylcholine (ACh) release from canine and equine airway tissues. Trachealis strips and bronchial segments were suspended in 2 ml tissue baths. ACh release was induced by electrical field stimulation (EFS), and its content in tissue bath liquid was measured by high pressure liquid chromatography (HPLC) with electrochemical detection. In canine airways, exogenous PGE2 (10(-9) to 10(-7) M) inhibited ACh release concentration-dependently, whereas inhibition of endogenous prostanoid production by indomethacin (3 x 10(-6) M) augmented ACh release. By contrast, in equine airways, exogenous PGE2 had no effect on ACh release in bronchi but at 10(-7) M augmented ACh release in the trachea. Cyclooxygenase inhibition by either indomethacin or meclofenamate (10(-6) M) did not influence ACh release. We conclude that exogenous PGE2 and endogenous prostanoids inhibit ACh release from cholinergic nerves in canine but not equine airways.
Publication Date: 1994-11-01 PubMed ID: 7846106DOI: 10.1016/0952-3278(94)90007-8Google Scholar: Lookup
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- Comparative Study
- Journal Article
- Research Support
- U.S. Gov't
- P.H.S.
Summary
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The research investigates the impact of a substance called prostaglandin E2 (PGE2) on the release of acetylcholine (ACh) from nerves in canine and equine airways. Results indicate that PGE2 and prostanoids can inhibit the release of ACh in dogs but not horses.
Objective and Methodology of Study
- The main objective of this study was to investigate the effects of PGE2 and endogenous prostanoids on the release of Acetylcholine (ACh) from the airways of dogs and horses. ACh is a key neurotransmitter, and its regulation can impact the function of the respiratory system.
- To measure the release of ACh, the study used trachealis (a muscle strip from the trachea) and bronchial segments from both types of animals. These tissue samples were suspended in small tissue baths.
- The release of ACh was triggered artificially using a method called electrical field stimulation (EFS). High-pressure liquid chromatography (HPLC) with electrochemical detection was used to measure the ensuing ACh content in the tissue bath liquid.
Key Findings
- In the case of dogs, it was observed that the introduction of exogenous PGE2 concentration-dependently inhibited the release of ACh. Furthermore, it was discovered that the inhibition of the natural production of prostanoids by a drug called indomethacin increased the release of ACh.
- Contrarily, for horses, exogenous PGE2 had no effect on ACh release in bronchi. However, at a certain concentration (10(-7) M), it enhanced ACh release in the trachea. Inhibiting cyclooxygenase, an enzyme responsible for the formation of prostanoids, had no notable influence on ACh release.
Conclusion of the Study
- The study concludes that both exogenous PGE2 and endogenous prostanoids suppress the release of Acetylcholine from cholinergic nerves in the airways of dogs but show no inhibitory effect in horses.
This research could have implications for understanding and potentially treating respiratory issues in these species.
Cite This Article
APA
Zhao WW, Robinson NE, Yu MF.
(1994).
PGE2 inhibits acetylcholine release from cholinergic nerves in canine but not equine airways.
Prostaglandins Leukot Essent Fatty Acids, 51(5), 347-355.
https://doi.org/10.1016/0952-3278(94)90007-8 Publication
Researcher Affiliations
- Department of Physiology, Michigan State University, East Lansing 48824.
MeSH Terms
- Acetylcholine / metabolism
- Animals
- Bronchi / innervation
- Bronchi / metabolism
- Chromatography, High Pressure Liquid
- Cyclooxygenase Inhibitors / pharmacology
- Dinoprostone / pharmacology
- Dogs
- Electric Stimulation
- Female
- Horses
- Indomethacin / pharmacology
- Male
- Meclofenamic Acid / pharmacology
- Species Specificity
- Trachea / innervation
- Trachea / metabolism
Grant Funding
- HL-49494 / NHLBI NIH HHS
Citations
This article has been cited 2 times.- af Forselles KJ, Root J, Clarke T, Davey D, Aughton K, Dack K, Pullen N. In vitro and in vivo characterization of PF-04418948, a novel, potent and selective prostaglandin EP₂ receptor antagonist.. Br J Pharmacol 2011 Dec;164(7):1847-56.
- Peters T, Henry PJ. Protease-activated receptors and prostaglandins in inflammatory lung disease.. Br J Pharmacol 2009 Oct;158(4):1017-33.
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