Decreased mononuclear cell beta-adrenergic receptors in bronchial asthma: parallel studies of lymphocyte and granulocyte desensitization

Yasuyuki Sano, Gavin Watt, R. G. Townley

Research output: Contribution to journalArticle

42 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)495-503
Number of pages9
JournalJournal of Allergy and Clinical Immunology
Volume72
Issue number5 PART 1
DOIs
StatePublished - 1983

Fingerprint

Receptors, Adrenergic, beta
Granulocytes
Asthma
Lymphocytes
Mononuclear Leukocytes
Adrenergic beta-Agonists
Neutrophils
Pharmaceutical Preparations
Terbutaline
Control Groups
Group Psychotherapy
Psychologic Desensitization
Leukocytes
Cell Membrane
Membranes

All Science Journal Classification (ASJC) codes

  • Immunology
  • Immunology and Allergy

Cite this

Decreased mononuclear cell beta-adrenergic receptors in bronchial asthma : parallel studies of lymphocyte and granulocyte desensitization. / Sano, Yasuyuki; Watt, Gavin; Townley, R. G.

In: Journal of Allergy and Clinical Immunology, Vol. 72, No. 5 PART 1, 1983, p. 495-503.

Research output: Contribution to journalArticle

@article{db8925568d2142dcb50f4d1c39b02696,
title = "Decreased mononuclear cell beta-adrenergic receptors in bronchial asthma: parallel studies of lymphocyte and granulocyte desensitization",
abstract = "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.",
author = "Yasuyuki Sano and Gavin Watt and Townley, {R. G.}",
year = "1983",
doi = "10.1016/0091-6749(83)90587-0",
language = "English",
volume = "72",
pages = "495--503",
journal = "Journal of Allergy and Clinical Immunology",
issn = "0091-6749",
publisher = "Mosby Inc.",
number = "5 PART 1",

}

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.

PY - 1983

Y1 - 1983

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 -