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Am J Physiol Lung Cell Mol Physiol 265: L389-L394, 1993;
1040-0605/93 $5.00
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AJP - Lung Cellular and Molecular Physiology, Vol 265, Issue 4 389-L394, Copyright © 1993 by American Physiological Society

ARTICLES

Visualization of high- and low-affinity beta-adrenergic receptors in rat lung: upregulation by chronic hypoxia

D. J. Birnkrant, P. B. Davis and P. Ernsberger
Department of Pediatrics, Rainbow Babies and Children's Hospital, Cleveland, Ohio.

Chronic hypoxia induces a hyperadrenergic state which down-regulates beta-adrenergic receptors (beta-AR) in the heart. We visualized lung beta-AR binding sites after adaptation to chronic hypoxia by autoradiography of whole lung sections labeled with 50 pM 125I-labeled pindolol. A low concentration of agonist (32 nM isoproterenol) selectively masked beta-ARs with high affinity for agonists. Total specific beta-AR binding increased twofold with hypoxia. In both the control and hypoxic lung sections, 60-70% of the beta-ARs were in a high-affinity state, which could be reversed by guanine nucleotide. Autoradiography revealed a high density of high- and low-affinity beta-AR sites in lung parenchyma, predominantly involving alveolar walls, but also the walls of airways and blood vessels. The distribution of high- and low-affinity beta-AR within the lung was qualitatively identical. Hypoxia increased beta-AR binding without affecting its distribution. The majority of the additional beta-ARs induced during adaptation to chronic hypoxia are in the high-affinity state, and are thus of probable functional significance.


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