| Beta2-adrenergic stimulation blunts inhibition of epithelial ion transport by hypoxia of rat alveolar epithelial cells. | |
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MedLine Citation:
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PMID: 20054151 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Hypoxia impairs alveolar fluid clearance by inhibition of Na(+) reabsorption, and also impairs beta(2) adrenergic signaling in alveolar epithelium. Since both are major rescue mechanisms preventing pulmonary edema, we studied whether acute and prolonged treatment with terbutaline would prevent hypoxic inhibition of ion transport. Short circuit currents (ISC) were measured on normoxic and hypoxic (1.5% O(2); 24h) primary rat alveolar type II (ATII) cells in absence and presence of terbutaline (1 to 100 microM, 24h). Control and pre-treated cells were stimulated acutely with terbutaline. Transepithelial transport was measured as short circuit current (ISC) in Ussing chambers. Terbutaline induced a rapid decrease ISC (-20%) followed by a slow raise. The transient change in ISC was not inhibited by amiloride but was prevented after Cl(-) depletion indicating a Cl(-) current. The slow increase after this transient was amiloride-sensitive indicating a Na(+) current. Total ISC, its amiloride-sensitive component, and the transient decrease upon terbutaline stimulation were decreased by hypoxia. 24h treatment with terbutaline stimulated these currents in normoxia and hypoxia, although stimulation was less in the latter. 24h treatment with terbutaline increased the capacity of Na(+)/K(+)-ATPase and ENaC as measured after permeabilization with amphotericin. These changes were not paralleled by altered mRNA expression. Acutely applied terbutaline induced a 4-fold increase in cAMP formation in normoxia; terbutaline-induced cAMP-formation was impaired by hypoxia (-20%). Pre-treatment with terbutaline for 24h decreased terbutaline-induced cAMP formation by 85%. Despite this desensitization, addition of terbutaline to terbutaline pre-treated cells caused a larger increase in Cl(-) and Na(+) transport both in normoxia and hypoxia than in non pre-treated cells. These results indicate that beta(2) adrenergic stimulation increased Na(+)- and Cl(-) transport in ATII cells even in hypoxia thus restoring normal reabsorption. |
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Authors:
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Benjamin Loeh; Emel Baloglu; Alberto Ke; Peter B?rtsch; Heimo Mairb?url |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-12-22 |
Journal Detail:
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Title: Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology Volume: 25 ISSN: 1421-9778 ISO Abbreviation: Cell. Physiol. Biochem. Publication Date: 2010 |
Date Detail:
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Created Date: 2010-01-07 Completed Date: 2010-02-25 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9113221 Medline TA: Cell Physiol Biochem Country: Switzerland |
Other Details:
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Languages: eng Pagination: 123-34 Citation Subset: IM |
Copyright Information:
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2010 S. Karger AG, Basel |
Affiliation:
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Medical Clinic VII, Sports Medicine, University Hospital Heidelberg, Heidelberg, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adrenergic beta-Agonists
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pharmacology* Animals Cell Hypoxia / drug effects* Cells, Cultured Ion Transport / drug effects* Male Pneumocytes / drug effects*, metabolism Rats Rats, Sprague-Dawley Receptors, Adrenergic, beta-2 / agonists, metabolism* Terbutaline / pharmacology* |
| Chemical | |
Reg. No./Substance:
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0/Adrenergic beta-Agonists; 0/Receptors, Adrenergic, beta-2; 23031-25-6/Terbutaline |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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