Abstract |
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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Authors | D J Birnkrant, P B Davis, P Ernsberger |
Journal | The American journal of physiology
(Am J Physiol)
Vol. 265
Issue 4 Pt 1
Pg. L389-94
(Oct 1993)
ISSN: 0002-9513 [Print] United States |
PMID | 8238373
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Receptors, Adrenergic, beta
- Guanylyl Imidodiphosphate
- Sodium
- Pindolol
- Isoproterenol
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Topics |
- Animals
- Autoradiography
- Chronic Disease
- Guanylyl Imidodiphosphate
(pharmacology)
- Hypoxia
(metabolism)
- Isoproterenol
(pharmacology)
- Lung
(metabolism)
- Male
- Pindolol
(antagonists & inhibitors, metabolism)
- Rats
- Rats, Wistar
- Receptors, Adrenergic, beta
(metabolism)
- Reference Values
- Sodium
(pharmacology)
- Up-Regulation
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