Distribution of β1‐ and β2‐adrenoceptors in mouse trachea and lung: a quantitative autoradiographic study

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Abstract
Binding and quantitative autoradiography were used to detect [125I]‐iodocyanopindolol (I‐CYP) associated with β1‐ and β2‐adrenoceptors in mouse tracheal epithelium and airway smooth muscle as well as in lung parenchymal tissue. Specific I‐CYP binding to slide‐mounted tissue sections of both trachea and parenchyma was of high affinity (KD = 49.0 pm, n = 3, trachea; KD = 118.9 pm, n = 3, parenchyma) and saturable, involving single populations of non‐interacting binding sites (Hill coefficient nH = 1.00 ± 0.02, trachea; nH = 0.99 ± 0.03, parenchyma). Direct measurement of tissue radioactivity also showed that specific I‐CYP binding was competitively inhibited in the presence of the β‐adrenoceptor antagonists (−)‐propranolol (non‐selective), CGP 20712A (β1‐selective) and ICI 118,551 (β2‐selective). Analysis of the competition binding curves for the two selective antagonists revealed mixed populations of β1‐ and β2‐adrenoceptors in the approximate proportions 33% and 67% respectively in mouse trachea and 28% and 72% respectively in mouse lung parenchyma. Densities of autoradiographic grains derived from specific I‐CYP binding to alveolar wall tissue and to tracheal epithelium and airway smooth muscle were quantified by a computer‐assisted image analysis system, which allowed the construction of competition binding curves in the presence of the selective β‐adrenoceptor antagonists CGP 20712A and ICI 118,551. Analysis of these data demonstrated that in alveolar wall, β1‐ and β2‐adrenoceptors co‐existed in the proportions 18% and 82%, respectively. Quantitative autoradiographic analyses also showed that β1‐ and β2‐adrenoceptors were differentially distributed in tracheal epithelium and airway smooth muscle. The β2‐adrenoceptor subtype accounted for 71% of all β‐adrenoceptors in epithelium. Conversely, β1‐adrenoceptors which mediate relaxant responses of mouse trachea to β‐adrenoceptor agonists (Henry & Goldie, 1990), accounted for 69% of all β‐adrenoceptors in the airway smooth muscle.
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