Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2008 Feb;38(2):127-34.
doi: 10.1165/rcmb.2007-0198TR. Epub 2007 Aug 20.

Alveolar epithelial beta2-adrenergic receptors

Gökhan M Mutlu  1 , Phillip Factor
Affiliations
Review

Alveolar epithelial beta2-adrenergic receptors

Gökhan M Mutlu et al. Am J Respir Cell Mol Biol. 2008 Feb.

Abstract

beta(2)-adrenergic receptors are present throughout the lung, including the alveolar airspace, where they play an important role for regulation of the active Na(+) transport needed for clearance of excess fluid out of alveolar airspace. beta(2)-adrenergic receptor signaling is required for up-regulation of alveolar epithelial active ion transport in the setting of excess alveolar edema. The positive, protective effects of beta(2)-adrenergic receptor signaling on alveolar active Na(+) transport in normal and injured lungs provide substantial support for the use of beta-adrenergic agonists to accelerate alveolar fluid clearance in patients with cardiogenic and noncardiogenic pulmonary edema. In this review, we summarize the role of beta(2)-adrenergic receptors in the alveolar epithelium with emphasis on their role in the regulation of alveolar active Na(+) transport in normal and injured lungs.

PubMed Disclaimer

Figures

<b>Figure 1.</b>
Figure 1.
Effects of β2-adrenergic receptor activation in alveolar epithelial cells. Activation of β2-adrenergic receptor (β2AR) increases alveolar active Na+ transport via upregulation of epithelial Na+ channel (ENaC) and cystic fibrosis transmembrane conductance regulator (CFTR) as well as basolaterally located Na,K-ATPase (open arrows). Activation of the receptor also increases β-catenin and surfactant release, which might be important in the pathogenesis/resolution of acute lung injury. ATP, adenosine triphosphate; cAMP, cyclic adenosine monophosphate; PKA, protein kinase A.
<b>Figure 2.</b>
Figure 2.
Proposed interaction of β2-adrenergic receptor with CFTR and other proteins. In the cell membrane, the β2AR is in close proximity to transport molecules such as CFTR and possibly ENaC. This macromolecular complex is maintained through interactions of the β2AR with scaffold and adaptor proteins including EBP50 and ezrin, which also link the receptor with submembrane cytoskeletal elements. ATP, adenosine triphosphate; cAMP, cyclic adenosine monophosphate; EBP50, ezrin-radixin-moesin-binding phosphoprotein 50; PKA, protein kinase A. (Adapted from Reference .)
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Mutlu GM, Koch WJ, Factor P. Alveolar epithelial beta 2-adrenergic receptors: their role in regulation of alveolar active sodium transport. Am J Respir Crit Care Med 2004;170:1270–1275. - PubMed
    1. Granneman JG. The putative beta4-adrenergic receptor is a novel state of the beta1-adrenergic receptor. Am J Physiol Endocrinol Metab 2001;280:E199–E202. - PubMed
    1. Spina D, Rigby PJ, Paterson JW, Goldie RG. Autoradiographic localization of beta-adrenoceptors in asthmatic human lung. Am Rev Respir Dis 1989;140:1410–1415. - PubMed
    1. Carstairs JR, Nimmo AJ, Barnes PJ. Autoradiographic visualization of beta-adrenoceptor subtypes in human lung. Am Rev Respir Dis 1985;132:541–547. - PubMed
    1. Liebler JM, Borok Z, Li X, Zhou B, Sandoval AJ, Kim KJ, Crandall ED. Alveolar epithelial type I cells express beta2-adrenergic receptors and G-protein receptor kinase 2. J Histochem Cytochem 2004;52:759–767. - PubMed

Publication types

MeSH terms

Substances