PubMed1985
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 adenosine 3',5'-cyclic monophosphate 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 less than 0.05), indicating increased sensitivity. However, 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. These data suggest that the autonomic aberrations associated with asthma do not extend to the alpha 2-adrenergic system of the platelet, and that the alpha 1-adrenergic hypersensitivity cannot be attributed to medication use or pulmonary dysfunction, but might be an intrinsic property of the disease.