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Pre- and postjunctional effects of inflammatory mediators in horse airways.
Abstract: In addition to their direct contractile effects, histamine (Hist), serotonin [5-hydroxytryptamine (5-HT)], and leukotriene (LT) D(4), in low concentrations, dramatically augment electrical field stimulation (EFS)-induced smooth muscle contractions in equine airways. To determine the mechanism of their action, we studied, in trachealis strips, the effect of these mediators on both cholinergically induced tension and the release of ACh from cholinergic nerves. All three mediators synergistically augmented the contraction of the trachealis that was due to release of endogenous ACh, i.e., EFS-induced contraction. These same mediators caused only a small but parallel shift of the ACh concentration-response curve. Comparison of the mediator effects on the responses to endogenous and exogenous ACh suggested a prejunctional effect. However, release of ACh was augmented only by Hist and 5-HT but not by LTD(4). Hist-induced contraction of trachealis was abolished by pyrilamine (H(1)-receptor antagonist) but not by ranitidine (H(2)-receptor antagonist), whereas thioperamide (H(3)-receptor antagonist) shifted the Hist response curve to the left. The augmenting effect of Hist on EFS-induced contraction was abolished by pyrilamine and unaffected by ranitidine or thioperamide. We conclude that inflammatory mediators can increase endogenous cholinergic responses of equine airways via both prejunctional and postjunctional mechanisms. LTD(4) acts solely on smooth muscle, whereas 5-HT and Hist additionally act on neuronal receptors to facilitate release of ACh. Excitatory effects of Hist, i.e., direct contractile effect, and augmentation of endogenous cholinergic response are both mediated via H(1) receptors, whereas the inhibitory H(3) receptors partially oppose the direct contractile effect of this mediator.
Publication Date: 1999-08-13 PubMed ID: 10444527DOI: 10.1152/ajplung.1999.277.2.L327Google Scholar: Lookup The Equine Research Bank provides access to a large database of publicly available scientific literature. Inclusion in the Research Bank does not imply endorsement of study methods or findings by Mad Barn.
- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.
The research investigates how inflammatory mediators, specifically histamine, serotonin, and leukotriene, influence the contraction of smooth muscles in horse airways, both directly and by enhancing the function of nerve-released acetylcholine. The study found that these mediators can heighten acetylcholine responses through both presynaptic (before the junction between nerve and muscle) and postsynaptic (after the junction) processes.
Study Design and Methods
- The research used trachealis strips, the smooth muscle of the horse windpipe, to study the effects of histamine, serotonin, and leukotriene.
- The goal was to identify how these mediators affect tension triggered by cholinergic activity (related to the neurotransmitter acetylcholine) and the release of acetylcholine from cholinergic nerves.
Results
- The three examined mediators were found to increase the contraction of trachealis by enhancing the action of naturally released acetylcholine.
- The mediators also caused a small shift in the concentration-response curve for acetylcholine, indicating an effect on how the muscle responded to this neurotransmitter.
- It was observed that augmentation of acetylcholine release was due to histamine and serotonin, but not leukotriene.
- The contractile impact of histamine on the trachealis muscle was cancelled by pyrilamine, an H1-histamine receptor antagonist, but unaffected by ranitidine, an H2-receptor antagonist. Thioperamide, an H3-receptor antagonist, caused the histamine response curve to shift to the left.
Conclusions
- The findings suggest that inflammatory mediators can enhance the natural cholinergic responses in horse airways via pre- and post-junctional mechanisms.
- Leukotriene D4 only influenced the smooth muscles, while serotonin and histamine acted on neuronal receptors, facilitating the release of acetylcholine.
- The effects of histamine in terms of direct contraction and amplification of natural cholinergic response are mediated by H1 receptors, while H3 receptors partially offset the contractile influence of histamine.
Cite This Article
APA
Olszewski MA, Zhang XY, Robinson NE.
(1999).
Pre- and postjunctional effects of inflammatory mediators in horse airways.
Am J Physiol, 277(2), L327-L333.
https://doi.org/10.1152/ajplung.1999.277.2.L327 Publication
Researcher Affiliations
- Departments of Large Animal Clinical Sciences and Physiology, Michigan State University, East Lansing, Michigan 48824-1314, USA.
MeSH Terms
- Acetylcholine / metabolism
- Acetylcholine / pharmacology
- Animals
- Electric Stimulation
- Female
- Histamine / pharmacology
- Horses / physiology
- In Vitro Techniques
- Inflammation Mediators / pharmacology
- Leukotriene D4 / pharmacology
- Male
- Muscle Contraction
- Muscle, Smooth / drug effects
- Muscle, Smooth / physiology
- Serotonin / pharmacology
- Trachea / drug effects
- Trachea / physiology
Citations
This article has been cited 2 times.- Schlenz H, Kummer W, Jositsch G, Wess J, Krasteva G. Muscarinic receptor-mediated bronchoconstriction is coupled to caveolae in murine airways. Am J Physiol Lung Cell Mol Physiol 2010 May;298(5):L626-36.
- Leduc L, Leclère M, Gauthier LG, Marcil O, Lavoie JP. Severe asthma in horses is associated with increased airway innervation. J Vet Intern Med 2024 Jan-Feb;38(1):485-494.
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