1 Bronchial smooth muscle, skeletal muscle and cardiac 13-adrenoceptor antagonism have been compared in twelve asthmatic patients after three 0-adrenoceptor antagonists at two dose levels. The non-selective antagonist propranolol (40 and 160 mg), the non-selective antagonist with partial agonist activity pindolol (5 and 20mg) and the Pl-selective antagonist atenolol (50 and 200 mg) were studied on separate occasions. 2 Six placebo days were used in this double-blind crossover study to allow interpretation of individual as well as group results. 3 Bronchial smooth muscle effects were assessed by resting spirometry, histamine inhalation test and spirometric response to inhaled fenoterol. Skeletal muscle effects were assessed by resting tremor and fenoterol induced tremor.4 Cardiac P-adrenoceptor antagonism was assessed by measuring the effect on resting heart rate and on maximum heart rate in a standard exercise test. 5 Pindolol tended to cause least change from placebo in resting spirometry, caused significant tremor response, inhibited the fenoterol airway response, and tended to protect against inhaled histamine. 6 Atenolol 50 mg was the only drug to allow a fenoterol airway response similar to placebo. Atenolol increased the inhaled histamine responsiveness. 7 Propranolol 160 mg caused the most reduction in spirometry but also tended to cause the maximum reduction in exercise heart rate. Propranolol caused increased inhaled histamine responsiveness. 8 Initial sensitivity to inhaled histamine did not necessarily predict significant reduction in an asthmatics' spirometry by a j3-adrenoceptor antagonist. The effect of a 3-adrenoceptor antagonist on histamine responsiveness does not correspond to its effect on inhaled 132-adrenoceptor agonist responsiveness.

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