ALPHA-ADRENERGIC RESPONSES IN ASTHMA

Medication-free subjects with asthma who had normal pulmonary function were evaluated for .alpha.1-adrenergic sensitivity by determination of the dose of topical phenylephrine required for mydriasis and for .alpha.2-adrenergic responsiveness by determination of the inhibition by norepinephrine of cAMP synthesis in platelets. Asthmatic subjects required significantly lower concentrations of phenylephrine for mydriasis than normal individuals (1.20 .+-. 0.38% vs. 1.53 .+-. 0.57%, P < 0.05), indicating increased sensitivity. Platelet .alpha.2-adrenergic responses were normal in these same asthmatic subjects, as were .alpha.2-receptor number and antagonist affinity determined by Scatchard analysis of equilibrium binding of [3H]-yohimbine to platelet particulates. Apparently, the autonomic aberrations associated with asthma do not extend to the .alpha.2-adrenergic system of the platelet, the .alpha.1-adrenergic hypersensitivity evidently cannot be attributed to medication use or pulmonary dysfunction, but might be an intrinsic property of the disease.