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Terbutaline-induced desensitization in rabbit aorta in vitro
1College of Pharmacy, University of Oklahoma, Health Sciences Center, Oklahoma City 73190.
Artery
|January 1, 1993
Summary
Terbutaline, a beta 2-adrenergic agonist, causes homologous desensitization of beta-adrenergic receptors in rabbit aorta rings in vitro. This desensitization is concentration- and time-dependent and does not require extracellular calcium.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
Background:
- Beta-adrenergic agonists like terbutaline are used clinically.
- Understanding receptor desensitization is crucial for drug efficacy.
Purpose of the Study:
- To investigate the characteristics of terbutaline-induced beta-adrenergic receptor desensitization in vitro.
- To determine if specific agents can prevent this desensitization.
Main Methods:
- Endothelium-denuded rabbit aorta rings were incubated with terbutaline.
- Receptor desensitization was assessed by measuring relaxation responses to isoproterenol after phenylephrine-induced contraction.
- The role of extracellular calcium and the effect of verapamil, ketotifen, prednisolone, and nedocromil were evaluated.
Main Results:
- Terbutaline exposure led to reduced relaxation responses to isoproterenol, indicating beta-adrenergic receptor desensitization.
- The desensitization was found to be homologous, dependent on exposure time and concentration, and partially reversible.
- Development of desensitization did not require extracellular calcium and was not inhibited by the tested agents.
Conclusions:
- Terbutaline induces homologous beta-adrenergic receptor desensitization in isolated rabbit aorta in vitro.
- This process is concentration- and time-dependent, partially reversible, and independent of extracellular calcium.
- The tested agents (verapamil, ketotifen, prednisolone, nedocromil) did not block terbutaline-induced desensitization.