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 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.
Davis
P B
PB
Paget
G L
GL
Turi
V
V
D000293:Adolescent; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000328:Adult; D000527:Alprostadil; D001249:Asthma / Q000503:physiopathology*; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism; D000242:Cyclic AMP / Q000096:biosynthesis; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011458:Prostaglandins E / Q000494:pharmacology; D011680:Pupil / Q000187:drug effects; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism; D015016:Yohimbine / Q000097:blood
D000316:Adrenergic alpha-Agonists; D011458:Prostaglandins E; D011942:Receptors, Adrenergic, alpha; D010656:Phenylephrine; D015016:Yohimbine; D000242:Cyclic AMP; D000527:Alprostadil; D009638:Norepinephrine