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Title: Autoradiographic localization of beta-adrenoceptors in asthmatic human lung

Abstract

The autoradiographic distribution and density of beta-adrenoceptors in human non-diseased and asthmatic bronchi were investigated using (125I)iodocyanopindolol (I-CYP). Analysis of the effects of the beta-adrenoceptor antagonists on I-CYP binding demonstrated that betaxolol (20 nM, beta 1-selective) had no significant effect on specific grain density in either nonasthmatic or asthmatic human bronchus, whereas ICI-118551 (20 nM, beta 2-selective) inhibited I-CYP binding by 85 +/- 9% and 89 +/- 3%, respectively. Thus, homogeneous populations of beta 2-adrenoceptors existed in bronchi from both sources. Large populations of beta-adrenoceptors were localized to the bronchial epithelium, submucosal glands, and airway smooth muscle. Asthmatic bronchial tissue featured epithelial damage with exfoliated cells associated with luminal mucus plugs. A thickened basement membrane and airway smooth muscle hyperplasia were also evident. High levels of specific I-CYP binding were also detected over asthmatic bronchial smooth muscle, as assessed by autoradiography and quantitation of specific grain densities. Isoproterenol and fenoterol were 10- and 13-fold less potent, respectively, in bronchi from asthmatic lung than in those from nonasthmatic lung. However, this attenuated responsiveness to beta-adrenoceptor agonists was not caused by reduced beta-adrenoceptor density in asthmatic airways. A defect may exist in the coupling between beta-adrenoceptors and postreceptor mechanisms in severely asthmaticmore » lung.« less

Authors:
; ; ;  [1]
  1. (Univ. of Western Australia, Nedlands, Perth (Australia))
Publication Date:
OSTI Identifier:
5026080
Resource Type:
Journal Article
Resource Relation:
Journal Name: American Review of Respiratory Disease; (USA); Journal Volume: 140:5
Country of Publication:
United States
Language:
English
Subject:
59 BASIC BIOLOGICAL SCIENCES; ASTHMA; PATHOGENESIS; RECEPTORS; BIOLOGICAL LOCALIZATION; SYMPATHOMIMETICS; AUTORADIOGRAPHY; BIOCHEMICAL REACTION KINETICS; BRONCHI; IODINE 125; LUNGS; MAN; ANIMALS; AUTONOMIC NERVOUS SYSTEM AGENTS; BETA DECAY RADIOISOTOPES; BODY; DAYS LIVING RADIOISOTOPES; DISEASES; DRUGS; ELECTRON CAPTURE RADIOISOTOPES; INTERMEDIATE MASS NUCLEI; IODINE ISOTOPES; ISOTOPES; KINETICS; MAMMALS; MEMBRANE PROTEINS; NUCLEI; ODD-EVEN NUCLEI; ORGANIC COMPOUNDS; ORGANS; PRIMATES; PROTEINS; RADIOISOTOPES; REACTION KINETICS; RESPIRATORY SYSTEM; RESPIRATORY SYSTEM DISEASES; VERTEBRATES; 550901* - Pathology- Tracer Techniques

Citation Formats

Spina, D., Rigby, P.J., Paterson, J.W., and Goldie, R.G.. Autoradiographic localization of beta-adrenoceptors in asthmatic human lung. United States: N. p., 1989. Web. doi:10.1164/ajrccm/140.5.1410.
Spina, D., Rigby, P.J., Paterson, J.W., & Goldie, R.G.. Autoradiographic localization of beta-adrenoceptors in asthmatic human lung. United States. doi:10.1164/ajrccm/140.5.1410.
Spina, D., Rigby, P.J., Paterson, J.W., and Goldie, R.G.. Wed . "Autoradiographic localization of beta-adrenoceptors in asthmatic human lung". United States. doi:10.1164/ajrccm/140.5.1410.
@article{osti_5026080,
title = {Autoradiographic localization of beta-adrenoceptors in asthmatic human lung},
author = {Spina, D. and Rigby, P.J. and Paterson, J.W. and Goldie, R.G.},
abstractNote = {The autoradiographic distribution and density of beta-adrenoceptors in human non-diseased and asthmatic bronchi were investigated using (125I)iodocyanopindolol (I-CYP). Analysis of the effects of the beta-adrenoceptor antagonists on I-CYP binding demonstrated that betaxolol (20 nM, beta 1-selective) had no significant effect on specific grain density in either nonasthmatic or asthmatic human bronchus, whereas ICI-118551 (20 nM, beta 2-selective) inhibited I-CYP binding by 85 +/- 9% and 89 +/- 3%, respectively. Thus, homogeneous populations of beta 2-adrenoceptors existed in bronchi from both sources. Large populations of beta-adrenoceptors were localized to the bronchial epithelium, submucosal glands, and airway smooth muscle. Asthmatic bronchial tissue featured epithelial damage with exfoliated cells associated with luminal mucus plugs. A thickened basement membrane and airway smooth muscle hyperplasia were also evident. High levels of specific I-CYP binding were also detected over asthmatic bronchial smooth muscle, as assessed by autoradiography and quantitation of specific grain densities. Isoproterenol and fenoterol were 10- and 13-fold less potent, respectively, in bronchi from asthmatic lung than in those from nonasthmatic lung. However, this attenuated responsiveness to beta-adrenoceptor agonists was not caused by reduced beta-adrenoceptor density in asthmatic airways. A defect may exist in the coupling between beta-adrenoceptors and postreceptor mechanisms in severely asthmatic lung.},
doi = {10.1164/ajrccm/140.5.1410},
journal = {American Review of Respiratory Disease; (USA)},
number = ,
volume = 140:5,
place = {United States},
year = {Wed Nov 01 00:00:00 EST 1989},
month = {Wed Nov 01 00:00:00 EST 1989}
}