Beta-adrenergic responses in drug-free subjects with asthma

Abstract

Young atopic subjects with asthma who had taken no medication for 30 days and had normal pulmonary function were compared to atopic and nonatopic control subjects in several measures of β-adrenergic response. Subjects with asthma required a larger dose of infused isoproterenol (14.3 ± 3.9 ng/kg/min) to increase pulse pressure by a target >22 mm Hg than nonatopic control subjects (8.7 ± 3.3 ng/kg/min). Asymptomatic atopic control subjects had intermediate sensitivity (12.0 ± 6.0 ng/kg/min) (F = 3.67; p < 0.05). At the dose of infused isoproterenol producing the target pulse pressure response, the increase in low frequency (1 to 8 cycles per minute) heart rate variability was less in subjects with asthma (107 ± 34% increase in normal subjects versus 9 ± 21 % increase in subjects with asthma; p < 0.05). In addition, subjects with the least β-adrenergic responsiveness had the most reactive airways. Airway reactivity (assessed by the provocative concentration of methacholine causing a 20% fall in FEV 1) correlated with both the dose of isoproterenol required for the target pulse pressure response (R s = - 0.46; p < 0.05) and the isoproterenol-induced increase in low-frequency heart-rate variability (R s = 0.47; p < 0.05). In contrast, in lymphocytes and granulocytes from these same subjects, the cAMP response to isoproterenol and β-adrenergic receptor number were identical in normal subjects and subjects with asthma and unrelated to airway reactivity or to cardiovascular β-adrenergic responses. Thus, different results for β-adrenergic responsiveness in subjects with asthma are obtained in different tests in the same subjects.