1 The effects of single oral doses of atenolol 50 mg and xamoterol 200 mg ( a recently developed partial P1-adrenoceptor agonist) on lung function, heart rate and blood pressure were investigated in 11 patients with asthma. 2 Xamoterol caused a significant increase in heart rate and systolic blood pressure, which changes are consistent with the partial ,3l-adrenoceptor agonist activity of this drug.3 Atenolol induced a significant decrease in FEV1 and the forced vital capacity (FVC); there was a non-significant change in FEV1 and FVC after xamoterol. There was no significant difference between the effects of atenolol and xamoterol on FEV1 and FVC. 4 Bronchospasm induced by atenolol 50 mg and xamoterol 200 mg was completely reversed by inhalation of the P2-adrenoceptor agonist terbutaline to a cumulative dose of 4.0mg.

In order to localize the main site of action of the beta 2-adrenoceptor selective agonist terbutaline and the beta 1-adrenoceptor selective antagonist atenolol in the airways of asthmatic patients, we compared the effects of these drugs on maximal expiratory flow-volume (MEFV) curves when breathing air and when breathing a helium-oxygen (HeO2) mixture. To investigate whether a shift in localization of the bronchodilator effect occurs when terbutaline is inhaled repeatedly, dose-response curves with terbutaline were performed for parameters derived from MEFV curves when breathing air and for density dependence of expiratory airflow. By measurement of MEFV curves when the patients were breathing air alone, it was not possible to determine whether there is a difference in the bronchoconstrictor effect of atenolol between large and small airways. Inhalation of terbutaline to a cumulative dose of 2.0 mg induced a stepwise improvement in expiratory airflow parameters for large and small airways function when breathing air. Doubling the dose of inhaled terbutaline to 4 mg did not result in any further improvement of lung function. Neither atenolol nor terbutaline induced significant mean changes in density dependence of expiratory airflow. This was partly due to large inter- and intra-individual variations of this parameter. Another possibility is that atenolol and terbutaline effect large and small airways function equally.