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Effect of chronic nadolol treatment on isoproterenol induced mouse tracheal relaxation
Author(s) -
Lin Rui,
Knoll Brian J.,
Bond Richard A.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.918.7
Subject(s) - nadolol , ovalbumin , medicine , downregulation and upregulation , pertussis toxin , bronchoconstriction , endocrinology , lung , receptor , asthma , pharmacology , chemistry , anesthesia , immunology , antigen , g protein , biochemistry , propranolol , gene
Upregulation of Gi protein has been observed in animal models of asthma, and is associated with the impairment of isoproterenol (ISO) induced tracheal relaxation. Using an antigen driven mouse model of asthma, we investigated the effect of chronic nadolol treatment on ISO induced tracheal relaxation. The relaxant response of tracheal rings was tested in organ chamber. PKCα translocation and PLCβ1 expression in lung or bronchi homogenates were also evaluated by western blotting. ISO induced relaxations were impaired in contracted trachea from mice sensitized and challenged with ovalbumin (s/c mice) compared to trachea from control mice. Twelve hours incubation with 0.3 μg/ml pertussis toxin (PTX) resulted in a 20% increase of ISO induced relaxation in s/c mice, which was not observed in control mice. However, chronic nadolol treatment diminished this effect of PTX on s/c mice. Chronic nadolol treatment also decreased PLCβ1 in trachea and major bronchi homogenates though no effect was observed in the elevated translocation of PKCα in s/c mice. Our results suggested that chronic nadolol treatment may decrease β 2 ‐AR‐Gi coupling and Gq signaling in s/c mice.