TY - JOUR
T1 - Alpha- and beta-adrenergic-receptor systems in bronchial asthma and in subjects without asthma
T2 - Reduced mononuclear cell beta-receptors in bronchial asthma
AU - Sato, Toshio
AU - Bewtra, Againdra K.
AU - Hopp, Russell J.
AU - Nair, Nicki
AU - Townley, Robert G.
N1 - Funding Information:
From the Allergic Disease Center, Department of Medicine, Creigh-ton University School of Medicine, Omaha, Neb. Supported in part by National Institute of Allergy and Infectious Diseases, and the American Lung Association of Nebraska. Received for publication Aug. 8, 1989. Revised April 4, 1990. Accepted for publication June 19, 1990. Reprint requests: Robert G. Townley, MD, Creighton University Allergic Disease Center, 2500 California St., Omaha, NE 68178.
PY - 1990/12
Y1 - 1990/12
N2 - We assessed the adrenergic-receptor system in individuals with bronchial hyperreactivity. β-Adrenergic receptors on mononuclear cell membranes, α-adrenergic receptors on platelet membranes, and the cAMP response in these cell types to different stimuli, including platelet-activating factor (PAF), were determined. Studies were assessed in 10 subjects with mild asthma, six methacholine-sensitive subjects without asthma, and 10 normal subjects. The density and affinity of β-receptors and α-receptors were determined by Scatchard analysis. Our findings were that (1) subjects with asthma had a significantly lower density of β-receptors compared to normal subjects, (2) subjects with asthma had a significantly lower cAMP response to isoproterenol stimulation compared to the two other groups, (3) in subjects without asthma, PAF decreased the basal cAMP level and significantly inhibited the response to isoproterenol stimulation, (4) there was no difference in density and affinity of platelet α-receptors or in platelet cAMP responses to stimulation by α-agonists among these three groups, and (5) neither cAMP response or β-receptor density on mononuclear cells were significantly correlated with pulmonary-function tests (FEV1/FVC times 100), sensitivity to methacholine, or cold air inhalation. These results suggest that patients with asthma may have a lower isoproterenol cAMP response and decreased density of β-adrenergic receptors on mononuclear cells in the absence of β-agonist therapy. It is speculated that release of PAF and other mediators secondary to allergen exposure, even in the absence of overt attacks of asthma, may inhibit the response to endogenous or exogenous β-adrenergic agonists.
AB - We assessed the adrenergic-receptor system in individuals with bronchial hyperreactivity. β-Adrenergic receptors on mononuclear cell membranes, α-adrenergic receptors on platelet membranes, and the cAMP response in these cell types to different stimuli, including platelet-activating factor (PAF), were determined. Studies were assessed in 10 subjects with mild asthma, six methacholine-sensitive subjects without asthma, and 10 normal subjects. The density and affinity of β-receptors and α-receptors were determined by Scatchard analysis. Our findings were that (1) subjects with asthma had a significantly lower density of β-receptors compared to normal subjects, (2) subjects with asthma had a significantly lower cAMP response to isoproterenol stimulation compared to the two other groups, (3) in subjects without asthma, PAF decreased the basal cAMP level and significantly inhibited the response to isoproterenol stimulation, (4) there was no difference in density and affinity of platelet α-receptors or in platelet cAMP responses to stimulation by α-agonists among these three groups, and (5) neither cAMP response or β-receptor density on mononuclear cells were significantly correlated with pulmonary-function tests (FEV1/FVC times 100), sensitivity to methacholine, or cold air inhalation. These results suggest that patients with asthma may have a lower isoproterenol cAMP response and decreased density of β-adrenergic receptors on mononuclear cells in the absence of β-agonist therapy. It is speculated that release of PAF and other mediators secondary to allergen exposure, even in the absence of overt attacks of asthma, may inhibit the response to endogenous or exogenous β-adrenergic agonists.
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U2 - 10.1016/S0091-6749(05)80144-7
DO - 10.1016/S0091-6749(05)80144-7
M3 - Article
C2 - 2175758
AN - SCOPUS:0025679461
VL - 86
SP - 839
EP - 850
JO - Journal of Allergy and Clinical Immunology
JF - Journal of Allergy and Clinical Immunology
SN - 0091-6749
IS - 6 PART 1
ER -