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Text
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URL Address
<a href="http://doi.org/10.1152/ajplung.00339.2002" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajplung.00339.2002</a>
Pages
L578–583
Issue
3
Volume
285
Dublin Core
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Title
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Postreceptor defects in alveolar epithelial beta-adrenergic signaling after prolonged isoproterenol infusion.
Publisher
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American journal of physiology. Lung cellular and molecular physiology
Date
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2003
2003-09
Subject
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8-Bromo Cyclic Adenosine Monophosphate/pharmacology; Adenylyl Cyclases/metabolism; Adrenergic; Adrenergic beta-Agonists/*pharmacology; Animals; beta/*metabolism; Colforsin/pharmacology; Cyclic AMP-Dependent Protein Kinase Type II; Cyclic AMP-Dependent Protein Kinases/metabolism; Cyclic AMP/metabolism; Extravascular Lung Water/metabolism; Isoproterenol/*pharmacology; Male; Pulmonary Alveoli/*drug effects/*metabolism; Pulmonary Edema/metabolism; Rats; Receptors; Respiratory Mucosa/drug effects/metabolism; Signal Transduction/drug effects; Sprague-Dawley
Creator
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Morgan Eric E; Stader Sonya M; Hodnichak Cheryl M; Mavrich Kate E; Folkesson Hans G; Maron Michael B
Description
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We previously found that prolonged isoproterenol (Iso) infusion in rats impaired the ability of beta-adrenoceptor (beta-AR) agonists to increase alveolar liquid clearance (ALC). Here, we determined if postreceptor defects in beta-AR signaling contribute to this impairment. Iso was infused using subcutaneous miniosmotic pumps (4, 40, or 400 microg. kg-1. h-1) in rats for 48 h. At this time, forskolin-stimulated ALC was measured by mass balance. Forskolin-stimulated ALC [33.4 +/- 2.1%/h (mean +/- SE) in vehicle-infused rats] was reduced by 25 and 38%, respectively, after the 40 and 400 microg. kg-1. h-1 Iso infusions. The ability of forskolin to increase cAMP was reduced by 70% in alveolar type II (ATII) cells isolated from rats infused with 400 microg. kg-1. h-1 Iso. Additionally, the ability of the stable cAMP analog 8-bromoadenosine-3',5'-cyclic monophosphorothioate, Sp-isomer, to increase ALC (48.7 +/- 3.0% in vehicle-infused rats) was reduced by 25 and 51%, respectively, after the 40 and 400 microg. kg-1. h-1 infusions. Finally, the ability of cAMP to increase protein kinase A activity was eliminated in ATII cells isolated from rats infused with Iso at 400 microg. kg-1. h-1. These data demonstrate that prolonged beta-AR agonist exposure can impair alveolar epithelial beta-AR signaling downstream of the beta-AR.
Identifier
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<a href="http://doi.org/10.1152/ajplung.00339.2002" target="_blank" rel="noreferrer noopener">10.1152/ajplung.00339.2002</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2003
8-Bromo Cyclic Adenosine Monophosphate/pharmacology
Adenylyl Cyclases/metabolism
Adrenergic
Adrenergic beta-Agonists/*pharmacology
American journal of physiology. Lung cellular and molecular physiology
Animals
beta/*metabolism
Colforsin/pharmacology
Cyclic AMP-Dependent Protein Kinase Type II
Cyclic AMP-Dependent Protein Kinases/metabolism
Cyclic AMP/metabolism
Extravascular Lung Water/metabolism
Folkesson Hans G
Hodnichak Cheryl M
Isoproterenol/*pharmacology
Male
Maron Michael B
Mavrich Kate E
Morgan Eric E
Pulmonary Alveoli/*drug effects/*metabolism
Pulmonary Edema/metabolism
Rats
Receptors
Respiratory Mucosa/drug effects/metabolism
Signal Transduction/drug effects
Sprague-Dawley
Stader Sonya M