Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 839-850 |
| Number of pages | 12 |
| Journal | Journal of Allergy and Clinical Immunology |
| Volume | 86 |
| Issue number | 6 PART 1 |
| DOIs | |
| State | Published - 1990 |
| Externally published | Yes |
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All Science Journal Classification (ASJC) codes
- Immunology
- Immunology and Allergy
Cite this
Alpha- and beta-adrenergic-receptor systems in bronchial asthma and in subjects without asthma : Reduced mononuclear cell beta-receptors in bronchial asthma. / Sato, Toshio; Bewtra, Againdra K.; Hopp, Russell J.; Nair, Nicki; Townley, Robert G.
In: Journal of Allergy and Clinical Immunology, Vol. 86, No. 6 PART 1, 1990, p. 839-850.Research output: Contribution to journal › Article
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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.
PY - 1990
Y1 - 1990
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
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 -