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Modulation of ACh release from airway cholinergic nerves in horses with recurrent airway obstruction.
Abstract: To evaluate the functional status of neuronal alpha2-adrenoceptors (ARs) and beta2-ARs on ACh release in horses with recurrent airway obstruction (RAO), we examined the effects of the physiological agonists epinephrine (Epi) and norepinephrine (NE) and the beta2-agonists RR- and RR/SS-formoterol on ACh release from airway cholinergic nerves of horses with RAO. Because SS-formoterol, a distomer of the beta2-agonist, increases ACh release from airways of control horses only after the autoinhibitory muscarinic receptors are blocked by atropine, we also tested the hypothesis that if there is an M2-receptor dysfunction in equine RAO, SS-formoterol should increase ACh release even in the absence of atropine. ACh release was evoked by electrical field stimulation and measured by HPLC. Epi and NE caused less inhibition of ACh release in horses with RAO than in control horses. At the catecholamine concentration achieved during exercise (10(-7) M), the inhibition induced by Epi and NE was 10.8 +/- 13.2 and 3.4 +/- 6.8%, respectively, in equine RAO versus 41.0 +/- 6.4 and 27.1 +/- 5.6%, respectively, in control horses. RR- and RR/SS-formoterol (10(-8) to 10(-5) M) increased ACh release to a similar magnitude as that in control horses. These results indicate that neuronal beta2-ARs are functioning; however, the alpha2-ARs are dysfunctional in the airways of horses with RAO in response to circulating catecholamines. SS-formoterol (10(-8) to 10(-5) M) facilitated ACh release in horses with RAO even in the absence of atropine. Addition of atropine did not cause significantly more augmentation of ACh release over the effect of SS-formoterol alone. The magnitude of augmentation in horses with RAO in the absence of atropine was similar to that in control horses in the presence of atropine. The latter observations could be explained by neuronal muscarinic-autoreceptor dysfunction in equine RAO.
Publication Date: 1999-05-18 PubMed ID: 10330033DOI: 10.1152/ajplung.1999.276.5.L769Google 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 researchers investigated the functionality of neuronal alpha2-adrenoceptors (ARs) and beta2-ARs in modulating Acetylcholine (ACh) release in the airways of horses suffering from recurrent airway obstruction (RAO). The study revealed that alpha2-ARs are dysfunctional, while neuronal beta2-ARs are functional. Additionally, the research indicated a possibility of neuronal muscarinic-autoreceptor dysfunction in RAO afflicted horses.
Objectives of the Research
- The study sought to understand the way ACh release is regulated in the airways of horses suffering from RAO.
- The focus was on the functionality of neuronal alpha2-adrenoceptors (ARs) and beta2-ARs and their ability to regulate ACh release.
Methodology and Key Findings
- The researchers triggered the release of Acetylcholine (ACh) by electrical field stimulation and it was quantified using High-Performance Liquid Chromatography (HPLC).
- The action of epinephrine (Epi) and norepinephrine (NE) — physiological alpha2-AR agonists— and RR- and RR/SS-formoterol —beta2-AR agonists— on ACh release was evaluated.
- The results showed that Epi and NE caused less inhibition of ACh release in horses with RAO than in healthy control horses, indicating a dysfunction of alpha2-ARs in RAO affected horses.
- RR- and RR/SS-formoterol increased ACh release similarly in both the groups, suggesting that beta2-ARs are functioning properly.
Investigating Potential M2-receptor Dysfunction
- The authors hypothesized that if there were an M2-receptor dysfunction in RAO affected horses, SS-formoterol should increase ACh release even without the presence of atropine, an M2 receptor blocker.
- Results showed that this was indeed the case, supporting their hypothesis of a potential M2-receptor dysfunction in RAO affected horses.
- The dialing up of ACh release by SS-formoterol in horses with RAO even without atropine was parallel to the reaction seen in control horses under the influence of atropine.
In conclusion, the study underscores the possibility of neuronal alpha2-ARs and M2 muscarinic-autoreceptor dysfunction in horses suffering from recurrent airway obstruction. This offers potential pathways for therapeutic intervention.
Cite This Article
APA
Zhang XY, Robinson NE, Zhu FX.
(1999).
Modulation of ACh release from airway cholinergic nerves in horses with recurrent airway obstruction.
Am J Physiol, 276(5), L769-L775.
https://doi.org/10.1152/ajplung.1999.276.5.L769 Publication
Researcher Affiliations
- Departments of Large Animal Clinical Sciences and Physiology, Michigan State University, East Lansing, Michigan 48824-1314, USA.
MeSH Terms
- Acetylcholine / metabolism
- Adrenergic alpha-Agonists / pharmacology
- Adrenergic beta-Agonists / pharmacology
- Animals
- Atropine / pharmacology
- Electric Stimulation
- Epinephrine / pharmacology
- Ethanolamines / pharmacology
- Formoterol Fumarate
- Horse Diseases / physiopathology
- Horses
- Lung Diseases, Obstructive / physiopathology
- Lung Diseases, Obstructive / veterinary
- Muscarinic Antagonists / pharmacology
- Norepinephrine / pharmacology
- Receptors, Adrenergic, alpha / physiology
- Receptors, Adrenergic, beta / physiology
- Recurrence
- Trachea / drug effects
- Trachea / innervation
Citations
This article has been cited 4 times.- Cheng S, Li L, He S, Liu J, Sun Y, He M, Grasing K, Premont RT, Suo WZ. GRK5 deficiency accelerates {beta}-amyloid accumulation in Tg2576 mice via impaired cholinergic activity. J Biol Chem 2010 Dec 31;285(53):41541-8.
- Moreno-Vinasco L, Verbout NG, Fryer AD, Jacoby DB. Retinoic acid prevents virus-induced airway hyperreactivity and M2 receptor dysfunction via anti-inflammatory and antiviral effects. Am J Physiol Lung Cell Mol Physiol 2009 Aug;297(2):L340-6.
- Verhein KC, Jacoby DB, Fryer AD. IL-1 receptors mediate persistent, but not acute, airway hyperreactivity to ozone in guinea pigs. Am J Respir Cell Mol Biol 2008 Dec;39(6):730-8.
- Vietmeier J, Niedorf F, Bäumer W, Martin C, Deegen E, Ohnesorge B, Kietzmann M. Reactivity of equine airways--a study on precision-cut lung slices. Vet Res Commun 2007 Jul;31(5):611-9.
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