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Beta-adrenergic receptor activity in ponies with recurrent obstructive pulmonary disease.

Abstract: Pulmonary function measurements were made in control ponies and in ponies with recurrent obstructive pulmonary disease (principals) during clinical remission and during an attack of acute airway obstruction. The ponies were given beta-adrenergic antagonists and agonists to determine the role of beta receptors in recurrent obstructive pulmonary disease, and to determine the subtypes of beta receptors mediating bronchodilation in ponies. Aerosol administration of the beta antagonists, propranolol (beta 1 and beta 2), atenolol (beta 1), and butoxamine (beta 2) decreased dynamic compliance (Cdyn) and increased pulmonary resistance (RL) in the principal ponies during airway obstruction, but were without effect when the ponies were in clinical remission. Intravenous administration of atropine reversed the effect of atenolol on Cdyn and RL, but was without effect on the decrease in Cdyn and increase in RL observed after butoxamine administration. The beta antagonists did not affect airway function in the control ponies. The effect of beta blockade on Cdyn and RL suggests beta-adrenergic activation in the central and peripheral airways of principal ponies, mediated through both beta 2- and beta 1-adrenergic receptors. The aerosol beta agonists, isoproterenol (beta 1 and beta 2), and clenbuterol (beta 2) attenuated histamine-induced airway obstruction to a similar extent in control ponies that were given histamine IV. In addition, the beta 1 antagonist, atenolol, did not attenuate the bronchodilation observed with isoproterenol. We concluded that, although beta 1- and beta 2-adrenergic receptors exist in pony airways and are activated during acute airway obstruction, bronchodilation in response to beta agonists in ponies seems to be mediated primarily by beta 2-adrenergic receptors.
Publication Date: 1991-09-01 PubMed ID: 1659260
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't
  • Research Support
  • U.S. Gov't
  • P.H.S.

Summary

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The research article investigates the role of beta-adrenergic receptors in ponies suffering from recurrent obstructive pulmonary disease. By testing the response of the disease under the influence of various beta receptor antagonists and agonists, the study concluded that bronchodilation in ponies is primarily mediated by beta 2-adrenergic receptors.

Understanding Recurrent Obstructive Pulmonary Disease in Ponies

  • The study looks at the pulmonary function in two groups of ponies: control ponies (healthy) and those with recurrent obstructive pulmonary disease (principals) both during a period of remission and during an acute airway obstruction attack.
  • Recurrent obstructive pulmonary disease (or ROPD) is a chronic condition affecting the respiratory system of horses, similar to conditions like asthma or COPD in humans. The disease causes inflammation and constriction of the airways, leading to difficulty in breathing.

Role of Beta-Adrenergic Receptors in ROPD

  • The researchers administered beta-adrenergic antagonists and agonists to the ponies to understand the role these beta receptors played in ROPD, and to identify the subtypes of beta receptors participating in bronchodilation, or the widening of bronchial tubes, in ponies.
  • The tests were conducted using various beta agonists and antagonists such as propranolol, atenolol, butoxamine, atropine, isoproterenol, and clenbuterol, to isolate and investigate the effects of both beta 1 and beta 2 receptors.

Results and Findings

  • In ponies experiencing airway obstruction due to ROPD, the administration of beta antagonists led to a decrease in dynamic compliance (Cdyn, a measure of the lung’s ability to expand) and an increase in pulmonary resistance (RL, opposition to airflow in the respiratory tract). In contrast, these beta antagonists had no effect when the ponies were in remission or in the control group of healthy ponies.
  • The differing effects of beta blockers on Cdyn and RL, and the reversal of these effects with the administration of other medications, suggested that the beta-adrenergic receptors play a significant role in the airways of ponies with ROPD.
  • The researchers concluded that while both beta 1 and beta 2 receptors are present and activated in pony airways during acute obstruction, the bronchodilation response to beta agonists seems to be primarily mediated by beta 2 receptors. This differential response to bronchodilation was confirmed via the administration of isoproterenol and clenbuterol, both of which showed similar mitigation of histamine-induced airway obstruction.

Cite This Article

APA
Scott JS, Berney CE, Derksen FJ, Robinson NE. (1991). Beta-adrenergic receptor activity in ponies with recurrent obstructive pulmonary disease. Am J Vet Res, 52(9), 1416-1422.

Publication

ISSN: 0002-9645
NlmUniqueID: 0375011
Country: United States
Language: English
Volume: 52
Issue: 9
Pages: 1416-1422

Researcher Affiliations

Scott, J S
  • Department of Large Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University, East Lansing 48824-1314.
Berney, C E
    Derksen, F J
      Robinson, N E

        MeSH Terms

        • Aerosols
        • Animals
        • Atenolol / administration & dosage
        • Atenolol / pharmacology
        • Butoxamine / administration & dosage
        • Butoxamine / pharmacology
        • Histamine / administration & dosage
        • Histamine / pharmacology
        • Horse Diseases / physiopathology
        • Horses
        • Isoproterenol / administration & dosage
        • Isoproterenol / pharmacology
        • Lung Diseases, Obstructive / physiopathology
        • Lung Diseases, Obstructive / veterinary
        • Propranolol / administration & dosage
        • Propranolol / pharmacology
        • Receptors, Adrenergic, beta / analysis
        • Receptors, Adrenergic, beta / drug effects
        • Receptors, Adrenergic, beta / physiology
        • Recurrence
        • Respiratory Function Tests / veterinary

        Grant Funding

        • HL01455 / NHLBI NIH HHS
        • HL27619 / NHLBI NIH HHS

        Citations

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