TY - JOUR
T1 - Decreased mononuclear cell beta-adrenergic receptors in bronchial asthma
T2 - parallel studies of lymphocyte and granulocyte desensitization
AU - Sano, Yasuyuki
AU - Watt, Gavin
AU - Townley, R. G.
N1 - Funding Information:
From the Allergic Disease Center, Department of Medicine, Creighton University, Omaha, Neb. This work was supported in part by NHLBI grant HL 24396 and NAIAD 5 p 50 AI 12029. Received for publication March 15, 1983. Accepted for publication June 9, 1983. Reprint requests: Dr. R. G. Townley, Allergic Disease Center, Creighton University, 2500 California St., Omaha, NE 68178.
PY - 1983/11
Y1 - 1983/11
N2 - To assess the interaction of bronchial asthma and beta-agonist drugs, beta-adrenergic receptors were measured in human mixed leukocyte, mononuclear cell, and polymorphonuclear leukocyte cell membranes simultaneously. The densities and affinities of beta-adrenergic receptors were determined, by Scatchard analysis, with a potent beta-antagonist 125I-hydroxybenzylpindolol (125I-HYP) and compared among 12 nonatopic controls (group I), 13 mild asthmatics not taking drugs (group II), and eight asthmatics receiving long-term beta-agonist therapy (group III). Our findings were as follows. (1) Asthmatics not taking drugs (group II) have significantly lower mean mononuclear leukocyte beta-adrenergic receptor density (p <0.05) but no significant difference in mean polymorphonuclear leukocyte beta-adrenergic receptor density than the control group. (2) Asthmatics receiving long-term beta-agonist treatment (group III) had significantly lower mean beta-adrenergic receptor density in all three cell fractions (p <0.05). (3) Group I and II females had a higher mean beta-adrenergic receptor density in mixed leukocyte and polymorphonuclear cell fractions than males (p <0.05). (4) Terbutaline sulfate clearly caused desensitization of beta-adrenergic receptors in human leukocyte membranes in vivo. These results show that beta-adrenergic receptor density is influenced by cell type, beta-adrenergic agonist administration, and sex; they also show that bronchial asthma itself is associated with lower lymphocyte beta-receptor density.
AB - To assess the interaction of bronchial asthma and beta-agonist drugs, beta-adrenergic receptors were measured in human mixed leukocyte, mononuclear cell, and polymorphonuclear leukocyte cell membranes simultaneously. The densities and affinities of beta-adrenergic receptors were determined, by Scatchard analysis, with a potent beta-antagonist 125I-hydroxybenzylpindolol (125I-HYP) and compared among 12 nonatopic controls (group I), 13 mild asthmatics not taking drugs (group II), and eight asthmatics receiving long-term beta-agonist therapy (group III). Our findings were as follows. (1) Asthmatics not taking drugs (group II) have significantly lower mean mononuclear leukocyte beta-adrenergic receptor density (p <0.05) but no significant difference in mean polymorphonuclear leukocyte beta-adrenergic receptor density than the control group. (2) Asthmatics receiving long-term beta-agonist treatment (group III) had significantly lower mean beta-adrenergic receptor density in all three cell fractions (p <0.05). (3) Group I and II females had a higher mean beta-adrenergic receptor density in mixed leukocyte and polymorphonuclear cell fractions than males (p <0.05). (4) Terbutaline sulfate clearly caused desensitization of beta-adrenergic receptors in human leukocyte membranes in vivo. These results show that beta-adrenergic receptor density is influenced by cell type, beta-adrenergic agonist administration, and sex; they also show that bronchial asthma itself is associated with lower lymphocyte beta-receptor density.
UR - http://www.scopus.com/inward/record.url?scp=0021083384&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0021083384&partnerID=8YFLogxK
U2 - 10.1016/0091-6749(83)90587-0
DO - 10.1016/0091-6749(83)90587-0
M3 - Article
C2 - 6313791
AN - SCOPUS:0021083384
VL - 72
SP - 495
EP - 503
JO - Journal of Allergy and Clinical Immunology
JF - Journal of Allergy and Clinical Immunology
SN - 0091-6749
IS - 5 PART 1
ER -