Upregulation of alveolar epithelial active Na+ transport is dependent on beta2-adrenergic receptor signaling
Alveolar epithelial beta-adrenergic receptor (betaAR) activation accelerates active Na+ transport in lung epithelial cells in vitro and speeds alveolar edema resolution in human lung tissue and normal and injured animal lungs. Whether these receptors are essential for alveolar fluid clearance (AFC)...
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| Veröffentlicht in: | Circulation research 2004-04, Vol.94 (8), p.1091-1100 |
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| creator | Mutlu, Gökhan M Dumasius, Vidas Burhop, James McShane, Pamela J Meng, Fan Jing Welch, Lynn Dumasius, Andrew Mohebahmadi, Nima Thakuria, Gloria Hardiman, Karen Matalon, Sadis Hollenberg, Steven Factor, Phillip |
| description | Alveolar epithelial beta-adrenergic receptor (betaAR) activation accelerates active Na+ transport in lung epithelial cells in vitro and speeds alveolar edema resolution in human lung tissue and normal and injured animal lungs. Whether these receptors are essential for alveolar fluid clearance (AFC) or if other mechanisms are sufficient to regulate active transport is unknown. In this study, we report that mice with no beta1- or beta2-adrenergic receptors (beta1AR-/-/beta2AR-/-) have reduced distal lung Na,K-ATPase function and diminished basal and amiloride-sensitive AFC. Total lung water content in these animals was not different from wild-type controls, suggesting that betaAR signaling may not be required for alveolar fluid homeostasis in uninjured lungs. Comparison of isoproterenol-sensitive AFC in mice with beta1- but not beta2-adrenergic receptors to beta1AR-/-/beta2AR-/- mice indicates that the beta2AR mediates the bulk of beta-adrenergic-sensitive alveolar active Na+ transport. To test the necessity of betaAR signaling in acute lung injury, beta1AR-/-/beta2AR-/-, beta1AR+/+/beta2AR-/-, and beta1AR+/+/beta2AR+/+ mice were exposed to 100% oxygen for up to 204 hours. beta1AR-/-/beta2AR-/- and beta1AR+/+/beta2AR-/- mice had more lung water and worse survival from this form of acute lung injury than wild-type controls. Adenoviral-mediated rescue of beta2-adrenergic receptor (beta2AR) function into the alveolar epithelium of beta1AR-/-/beta2AR-/- and beta1AR+/+/beta2AR-/- mice normalized distal lung beta2AR function, alveolar epithelial active Na+ transport, and survival from hyperoxia. These findings indicate that betaAR signaling may not be necessary for basal AFC, and that beta2AR is essential for the adaptive physiological response needed to clear excess fluid from the alveolar airspace of normal and injured lungs. |
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Whether these receptors are essential for alveolar fluid clearance (AFC) or if other mechanisms are sufficient to regulate active transport is unknown. In this study, we report that mice with no beta1- or beta2-adrenergic receptors (beta1AR-/-/beta2AR-/-) have reduced distal lung Na,K-ATPase function and diminished basal and amiloride-sensitive AFC. Total lung water content in these animals was not different from wild-type controls, suggesting that betaAR signaling may not be required for alveolar fluid homeostasis in uninjured lungs. Comparison of isoproterenol-sensitive AFC in mice with beta1- but not beta2-adrenergic receptors to beta1AR-/-/beta2AR-/- mice indicates that the beta2AR mediates the bulk of beta-adrenergic-sensitive alveolar active Na+ transport. To test the necessity of betaAR signaling in acute lung injury, beta1AR-/-/beta2AR-/-, beta1AR+/+/beta2AR-/-, and beta1AR+/+/beta2AR+/+ mice were exposed to 100% oxygen for up to 204 hours. beta1AR-/-/beta2AR-/- and beta1AR+/+/beta2AR-/- mice had more lung water and worse survival from this form of acute lung injury than wild-type controls. Adenoviral-mediated rescue of beta2-adrenergic receptor (beta2AR) function into the alveolar epithelium of beta1AR-/-/beta2AR-/- and beta1AR+/+/beta2AR-/- mice normalized distal lung beta2AR function, alveolar epithelial active Na+ transport, and survival from hyperoxia. These findings indicate that betaAR signaling may not be necessary for basal AFC, and that beta2AR is essential for the adaptive physiological response needed to clear excess fluid from the alveolar airspace of normal and injured lungs.</description><identifier>EISSN: 1524-4571</identifier><identifier>PMID: 15016730</identifier><language>eng</language><publisher>United States</publisher><subject>Amiloride - pharmacology ; Animals ; Biological Transport, Active - drug effects ; Biological Transport, Active - physiology ; Body Water - metabolism ; Cardiac Output ; Cyclic AMP - metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator - metabolism ; Epithelial Cells - drug effects ; Epithelial Cells - metabolism ; Genotype ; Humans ; Hyperoxia - physiopathology ; Ion Transport - drug effects ; Ion Transport - physiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Potassium Channels - metabolism ; Pulmonary Alveoli - drug effects ; Pulmonary Alveoli - injuries ; Pulmonary Alveoli - physiology ; Pulmonary Alveoli - physiopathology ; Receptors, Adrenergic, beta-1 - deficiency ; Receptors, Adrenergic, beta-1 - genetics ; Receptors, Adrenergic, beta-1 - physiology ; Receptors, Adrenergic, beta-2 - deficiency ; Receptors, Adrenergic, beta-2 - genetics ; Receptors, Adrenergic, beta-2 - physiology ; Recombinant Fusion Proteins - physiology ; Sodium - metabolism ; Sodium Channels - metabolism ; Sodium-Potassium-Exchanging ATPase - metabolism ; Specific Pathogen-Free Organisms ; Stroke Volume ; Transduction, Genetic</subject><ispartof>Circulation research, 2004-04, Vol.94 (8), p.1091-1100</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15016730$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mutlu, Gökhan M</creatorcontrib><creatorcontrib>Dumasius, Vidas</creatorcontrib><creatorcontrib>Burhop, James</creatorcontrib><creatorcontrib>McShane, Pamela J</creatorcontrib><creatorcontrib>Meng, Fan Jing</creatorcontrib><creatorcontrib>Welch, Lynn</creatorcontrib><creatorcontrib>Dumasius, Andrew</creatorcontrib><creatorcontrib>Mohebahmadi, Nima</creatorcontrib><creatorcontrib>Thakuria, Gloria</creatorcontrib><creatorcontrib>Hardiman, Karen</creatorcontrib><creatorcontrib>Matalon, Sadis</creatorcontrib><creatorcontrib>Hollenberg, Steven</creatorcontrib><creatorcontrib>Factor, Phillip</creatorcontrib><title>Upregulation of alveolar epithelial active Na+ transport is dependent on beta2-adrenergic receptor signaling</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>Alveolar epithelial beta-adrenergic receptor (betaAR) activation accelerates active Na+ transport in lung epithelial cells in vitro and speeds alveolar edema resolution in human lung tissue and normal and injured animal lungs. Whether these receptors are essential for alveolar fluid clearance (AFC) or if other mechanisms are sufficient to regulate active transport is unknown. In this study, we report that mice with no beta1- or beta2-adrenergic receptors (beta1AR-/-/beta2AR-/-) have reduced distal lung Na,K-ATPase function and diminished basal and amiloride-sensitive AFC. Total lung water content in these animals was not different from wild-type controls, suggesting that betaAR signaling may not be required for alveolar fluid homeostasis in uninjured lungs. Comparison of isoproterenol-sensitive AFC in mice with beta1- but not beta2-adrenergic receptors to beta1AR-/-/beta2AR-/- mice indicates that the beta2AR mediates the bulk of beta-adrenergic-sensitive alveolar active Na+ transport. To test the necessity of betaAR signaling in acute lung injury, beta1AR-/-/beta2AR-/-, beta1AR+/+/beta2AR-/-, and beta1AR+/+/beta2AR+/+ mice were exposed to 100% oxygen for up to 204 hours. beta1AR-/-/beta2AR-/- and beta1AR+/+/beta2AR-/- mice had more lung water and worse survival from this form of acute lung injury than wild-type controls. Adenoviral-mediated rescue of beta2-adrenergic receptor (beta2AR) function into the alveolar epithelium of beta1AR-/-/beta2AR-/- and beta1AR+/+/beta2AR-/- mice normalized distal lung beta2AR function, alveolar epithelial active Na+ transport, and survival from hyperoxia. These findings indicate that betaAR signaling may not be necessary for basal AFC, and that beta2AR is essential for the adaptive physiological response needed to clear excess fluid from the alveolar airspace of normal and injured lungs.</description><subject>Amiloride - pharmacology</subject><subject>Animals</subject><subject>Biological Transport, Active - drug effects</subject><subject>Biological Transport, Active - physiology</subject><subject>Body Water - metabolism</subject><subject>Cardiac Output</subject><subject>Cyclic AMP - metabolism</subject><subject>Cystic Fibrosis Transmembrane Conductance Regulator - metabolism</subject><subject>Epithelial Cells - drug effects</subject><subject>Epithelial Cells - metabolism</subject><subject>Genotype</subject><subject>Humans</subject><subject>Hyperoxia - physiopathology</subject><subject>Ion Transport - drug effects</subject><subject>Ion Transport - physiology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Potassium Channels - metabolism</subject><subject>Pulmonary Alveoli - drug effects</subject><subject>Pulmonary Alveoli - injuries</subject><subject>Pulmonary Alveoli - physiology</subject><subject>Pulmonary Alveoli - physiopathology</subject><subject>Receptors, Adrenergic, beta-1 - deficiency</subject><subject>Receptors, Adrenergic, beta-1 - genetics</subject><subject>Receptors, Adrenergic, beta-1 - physiology</subject><subject>Receptors, Adrenergic, beta-2 - deficiency</subject><subject>Receptors, Adrenergic, beta-2 - genetics</subject><subject>Receptors, Adrenergic, beta-2 - physiology</subject><subject>Recombinant Fusion Proteins - physiology</subject><subject>Sodium - metabolism</subject><subject>Sodium Channels - metabolism</subject><subject>Sodium-Potassium-Exchanging ATPase - metabolism</subject><subject>Specific Pathogen-Free Organisms</subject><subject>Stroke Volume</subject><subject>Transduction, Genetic</subject><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1kM1KxDAYRYMgzjj6CpKVGynkp2napQz-waCbcV2-Jl9rJJPGJB3w7R1QV3dxz7mLe0bWXIm6qpXmK3KZ8ydjvJaiuyArrhhvtGRr4t9jwmnxUNwc6DxS8EecPSSK0ZUP9A48BVPcEekr3NGSIOQ4p0JdphYjBouh0JM7YAFRgU0YME3O0IQGY5kTzW4K4F2Yrsj5CD7j9V9uyP7xYb99rnZvTy_b-10VVc0qYFwrzaRQg9RjZ6WSQ8ebWsLAoRkV64xoupYbCx3TgzBWgeWqbU89jnyUG3L7OxvT_LVgLv3BZYPeQ8B5yb3mbSt0K07gzR-4DAe0fUzuAOm7_79H_gBUDmGO</recordid><startdate>20040430</startdate><enddate>20040430</enddate><creator>Mutlu, Gökhan M</creator><creator>Dumasius, Vidas</creator><creator>Burhop, James</creator><creator>McShane, Pamela J</creator><creator>Meng, Fan Jing</creator><creator>Welch, Lynn</creator><creator>Dumasius, Andrew</creator><creator>Mohebahmadi, Nima</creator><creator>Thakuria, Gloria</creator><creator>Hardiman, Karen</creator><creator>Matalon, Sadis</creator><creator>Hollenberg, Steven</creator><creator>Factor, Phillip</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20040430</creationdate><title>Upregulation of alveolar epithelial active Na+ transport is dependent on beta2-adrenergic receptor signaling</title><author>Mutlu, Gökhan M ; Dumasius, Vidas ; Burhop, James ; McShane, Pamela J ; Meng, Fan Jing ; Welch, Lynn ; Dumasius, Andrew ; Mohebahmadi, Nima ; Thakuria, Gloria ; Hardiman, Karen ; Matalon, Sadis ; Hollenberg, Steven ; Factor, Phillip</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p540-a017570325b37f9d353b91643ab1a6f509c26981cda907b2cd5ad1588ab1ef1f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Amiloride - pharmacology</topic><topic>Animals</topic><topic>Biological Transport, Active - drug effects</topic><topic>Biological Transport, Active - physiology</topic><topic>Body Water - metabolism</topic><topic>Cardiac Output</topic><topic>Cyclic AMP - metabolism</topic><topic>Cystic Fibrosis Transmembrane Conductance Regulator - metabolism</topic><topic>Epithelial Cells - drug effects</topic><topic>Epithelial Cells - metabolism</topic><topic>Genotype</topic><topic>Humans</topic><topic>Hyperoxia - physiopathology</topic><topic>Ion Transport - drug effects</topic><topic>Ion Transport - physiology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Potassium Channels - metabolism</topic><topic>Pulmonary Alveoli - drug effects</topic><topic>Pulmonary Alveoli - injuries</topic><topic>Pulmonary Alveoli - physiology</topic><topic>Pulmonary Alveoli - physiopathology</topic><topic>Receptors, Adrenergic, beta-1 - deficiency</topic><topic>Receptors, Adrenergic, beta-1 - genetics</topic><topic>Receptors, Adrenergic, beta-1 - physiology</topic><topic>Receptors, Adrenergic, beta-2 - deficiency</topic><topic>Receptors, Adrenergic, beta-2 - genetics</topic><topic>Receptors, Adrenergic, beta-2 - physiology</topic><topic>Recombinant Fusion Proteins - physiology</topic><topic>Sodium - metabolism</topic><topic>Sodium Channels - metabolism</topic><topic>Sodium-Potassium-Exchanging ATPase - metabolism</topic><topic>Specific Pathogen-Free Organisms</topic><topic>Stroke Volume</topic><topic>Transduction, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mutlu, Gökhan M</creatorcontrib><creatorcontrib>Dumasius, Vidas</creatorcontrib><creatorcontrib>Burhop, James</creatorcontrib><creatorcontrib>McShane, Pamela J</creatorcontrib><creatorcontrib>Meng, Fan Jing</creatorcontrib><creatorcontrib>Welch, Lynn</creatorcontrib><creatorcontrib>Dumasius, Andrew</creatorcontrib><creatorcontrib>Mohebahmadi, Nima</creatorcontrib><creatorcontrib>Thakuria, Gloria</creatorcontrib><creatorcontrib>Hardiman, Karen</creatorcontrib><creatorcontrib>Matalon, Sadis</creatorcontrib><creatorcontrib>Hollenberg, Steven</creatorcontrib><creatorcontrib>Factor, Phillip</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mutlu, Gökhan M</au><au>Dumasius, Vidas</au><au>Burhop, James</au><au>McShane, Pamela J</au><au>Meng, Fan Jing</au><au>Welch, Lynn</au><au>Dumasius, Andrew</au><au>Mohebahmadi, Nima</au><au>Thakuria, Gloria</au><au>Hardiman, Karen</au><au>Matalon, Sadis</au><au>Hollenberg, Steven</au><au>Factor, Phillip</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of alveolar epithelial active Na+ transport is dependent on beta2-adrenergic receptor signaling</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2004-04-30</date><risdate>2004</risdate><volume>94</volume><issue>8</issue><spage>1091</spage><epage>1100</epage><pages>1091-1100</pages><eissn>1524-4571</eissn><abstract>Alveolar epithelial beta-adrenergic receptor (betaAR) activation accelerates active Na+ transport in lung epithelial cells in vitro and speeds alveolar edema resolution in human lung tissue and normal and injured animal lungs. Whether these receptors are essential for alveolar fluid clearance (AFC) or if other mechanisms are sufficient to regulate active transport is unknown. In this study, we report that mice with no beta1- or beta2-adrenergic receptors (beta1AR-/-/beta2AR-/-) have reduced distal lung Na,K-ATPase function and diminished basal and amiloride-sensitive AFC. Total lung water content in these animals was not different from wild-type controls, suggesting that betaAR signaling may not be required for alveolar fluid homeostasis in uninjured lungs. Comparison of isoproterenol-sensitive AFC in mice with beta1- but not beta2-adrenergic receptors to beta1AR-/-/beta2AR-/- mice indicates that the beta2AR mediates the bulk of beta-adrenergic-sensitive alveolar active Na+ transport. To test the necessity of betaAR signaling in acute lung injury, beta1AR-/-/beta2AR-/-, beta1AR+/+/beta2AR-/-, and beta1AR+/+/beta2AR+/+ mice were exposed to 100% oxygen for up to 204 hours. beta1AR-/-/beta2AR-/- and beta1AR+/+/beta2AR-/- mice had more lung water and worse survival from this form of acute lung injury than wild-type controls. Adenoviral-mediated rescue of beta2-adrenergic receptor (beta2AR) function into the alveolar epithelium of beta1AR-/-/beta2AR-/- and beta1AR+/+/beta2AR-/- mice normalized distal lung beta2AR function, alveolar epithelial active Na+ transport, and survival from hyperoxia. These findings indicate that betaAR signaling may not be necessary for basal AFC, and that beta2AR is essential for the adaptive physiological response needed to clear excess fluid from the alveolar airspace of normal and injured lungs.</abstract><cop>United States</cop><pmid>15016730</pmid><tpages>10</tpages></addata></record> |
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| ispartof | Circulation research, 2004-04, Vol.94 (8), p.1091-1100 |
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| subjects | Amiloride - pharmacology Animals Biological Transport, Active - drug effects Biological Transport, Active - physiology Body Water - metabolism Cardiac Output Cyclic AMP - metabolism Cystic Fibrosis Transmembrane Conductance Regulator - metabolism Epithelial Cells - drug effects Epithelial Cells - metabolism Genotype Humans Hyperoxia - physiopathology Ion Transport - drug effects Ion Transport - physiology Male Mice Mice, Inbred C57BL Mice, Knockout Potassium Channels - metabolism Pulmonary Alveoli - drug effects Pulmonary Alveoli - injuries Pulmonary Alveoli - physiology Pulmonary Alveoli - physiopathology Receptors, Adrenergic, beta-1 - deficiency Receptors, Adrenergic, beta-1 - genetics Receptors, Adrenergic, beta-1 - physiology Receptors, Adrenergic, beta-2 - deficiency Receptors, Adrenergic, beta-2 - genetics Receptors, Adrenergic, beta-2 - physiology Recombinant Fusion Proteins - physiology Sodium - metabolism Sodium Channels - metabolism Sodium-Potassium-Exchanging ATPase - metabolism Specific Pathogen-Free Organisms Stroke Volume Transduction, Genetic |
| title | Upregulation of alveolar epithelial active Na+ transport is dependent on beta2-adrenergic receptor signaling |
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