NDLI: β 1-Adrenoceptors compensate for β 3-adrenoceptors in ileum from β 3-adrenoceptor knock-out mice

Content Provider	PubMed Central
Author	Hutchinson, Dana S. Evans, Bronwyn A. Summers, Roger J.
Copyright Year	2001
Abstract	This study examines β1-, β2- and β3-adrenoceptor (AR)-mediated responses, mRNA levels and radioligand binding in ileum from β3-AR knock-out (−/−) (KO) and wild type (+/+) (FVB) mice. In KO and FVB mice, SR59230A (100 nM) (β3-AR antagonist) antagonized responses to (−)-isoprenaline in both KO and FVB mice. (−)-Isoprenaline mediated relaxation of ileum was antagonized weakly by ICI118551 (100 nM) (β2-AR antagonist). Responses to (−)-isoprenaline were more strongly antagonized by CGP20712A (100 nM) (β1-AR antagonist), propranolol (1 μM) (β1-/β2-AR antagonist), carvedilol (100 nM) (non-specific β-AR antagonist), and CGP12177A (100 nM) (β1-/β2-AR antagonist) in ileum from KO than in FVB mice. Responses to CL316243 (β3-AR agonist) in ileum from FVB mice were antagonized by SR59230A (100 nM) but not by propranolol (1 μM) or carvedilol (100 nM). CL316243 was ineffective in relaxing ileum from KO mice. CGP12177A had no agonist actions in ileum from either KO or FVB mice. β1-AR mRNA levels were increased 3 fold in ileum from KO compared to FVB mice. This was associated with an increased maximum number of β1-/β2-AR binding sites (Bmax). β2-AR mRNA levels were unaffected while no β3-AR mRNA was detected in KO mice. In mouse ileum, β3-ARs and to a lesser extent β1-ARs are the predominant adrenoceptor subtypes mediating relaxation in ileum from FVB mice. In KO mice β1-ARs functionally compensate for the lack of β3-ARs, and this is associated with increased β1-AR mRNA and levels of binding.
Related Links	http://dx.doi.org/10.1038/sj.bjp.0703828
Ending Page	442
Page Count	10
Starting Page	433
File Format	PDF
ISSN	00071188
Journal	British Journal of Pharmacology
Issue Number	2
Volume Number	132
Language	English
Publisher Date	2001-01-01
Access Restriction	Open
Subject Keyword	Pharmacology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Pharmacology

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