1. Maximal binding capacity (Bmax.) and the dissociation constant (KD) for the β-adrenoceptor antagonist 125I-cyanopindol were estimated in membrane preparations of hilar, lobar/main bronchi (level 1) and peripheral lung (level 11) of grossly normal lungs resected for bronchial carcinoma. The tissue distribution of 125I-cyanopindol-binding sites was assessed by autoradiography of complementary cryostat sections. The data obtained from the resections for carcinoma and bronchiectasis were used as disease controls for comparison with those obtained from patients with cystic fibrosis and asthma.

2. In carcinoma controls, mean Bmax. values (± sem) for airway levels 1 and 11 were 89 ± 4 and 133 ± 6 fmol/mg of protein, respectively (P <0.01). The corresponding KD values at each airway level were similar, i.e. 29 ± 2 and 33 ± 1 pmol/l, respectively. Autoradiography revealed that there was dense labelling of bronchial and bronchiolar epithelium and most strikingly of the alveolar wall.

3. Compared with carcinoma controls, mean Bmax. values in cystic fibrosis were significantly reduced in membrane preparations of both airway levels 1 and 11 (P <0.01). Autoradiography showed the reduction was most apparent in alveolar wall and bronchial epithelium.

4. There was a tendency to reduction of Bmax. in membrane preparations from patients with bronchiectasis at airway level I, but this failed to reach statistical significance. Autoradiography demonstrated that the density of labelling was significantly reduced in bronchial epithelium and bronchial smooth muscle as compared with carcinoma controls (P <0.01).

5. The Bmax. values were not significantly altered in membranes prepared from both airway levels in asthma, albeit there was a tendency towards reduction in Bmax. at level 1. At this level autoradiography demonstrated significantly reduced labelling of bronchial epithelium (P>0.01) and submucosal glands (P>0.05) but not of bronchial smooth muscle.

6. It is most likely that the reduction in β-adrenoceptor number that we have found in cystic fibrosis is secondary to pulmonary infection and airway inflammation. Its relationship to the primary defect remains unclear.

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