The influence of bumetanide on the membrane potential of mouse skeletal muscle cells in isotonic and hypertonic media
Increasing the medium osmolality, with a non‐ionic osmoticant, from control (289 mOsm) to 319 mOsm or 344 mOsm in the lumbrical muscle cell of the mouse, resulted in a depolarization of the membrane potential (Vm) of 5.9 mV and 10.9 mV, respectively. In control medium, the blockers of chloride relat...
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| Veröffentlicht in: | British journal of pharmacology 1997-01, Vol.120 (1), p.39-44 |
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| creator | Van Mil, H G J Geukes Foppen, R J Siegenbeek van Heukelom, J |
| description | Increasing the medium osmolality, with a non‐ionic osmoticant, from control (289 mOsm) to 319 mOsm or 344 mOsm in the lumbrical muscle cell of the mouse, resulted in a depolarization of the membrane potential (Vm) of 5.9 mV and 10.9 mV, respectively.
In control medium, the blockers of chloride related cotransport bumetanide and furosemide, induced a hyperpolarization of −3.6 and −3.0 mV and prevented the depolarization due to hypertonicity. When bumetanide was added in hypertonic media Vm fully repolarized to control values.
In a medium of 266 mOsm, the hyperpolarization by bumetanide was absent.
At 344 mOsm the half‐maximal effective concentration (IC50) was 0.5 μm for bumetanide and 21 μm for furosemide.
In solutions containing 1.25 mm sodium the depolarization by hypertonicity was reduced to 2.3 mV.
Reducing chloride permeability, by anthracene 9 carboxylic acid (9‐AC) in 289 mOsm, induced a small but significant hyperpolarization of −2.6 mV. Increasing medium osmolality to 344 mOsm enlarged this hyperpolarization significantly to −7.6 mV.
In a solution of 344 mOsm containing 100 μm ouabain, the bumetanide‐induced hyperpolarization of Vm was absent.
The results indicate that a Na‐K‐2Cl cotransporter is present in mouse lumbrical muscle fibre and that its contribution to Vm is dependent on medium osmolality.
British Journal of Pharmacology (1997) 120, 39–44; doi:10.1038/sj.bjp.0700887 |
| doi_str_mv | 10.1038/sj.bjp.0700887 |
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In control medium, the blockers of chloride related cotransport bumetanide and furosemide, induced a hyperpolarization of −3.6 and −3.0 mV and prevented the depolarization due to hypertonicity. When bumetanide was added in hypertonic media Vm fully repolarized to control values.
In a medium of 266 mOsm, the hyperpolarization by bumetanide was absent.
At 344 mOsm the half‐maximal effective concentration (IC50) was 0.5 μm for bumetanide and 21 μm for furosemide.
In solutions containing 1.25 mm sodium the depolarization by hypertonicity was reduced to 2.3 mV.
Reducing chloride permeability, by anthracene 9 carboxylic acid (9‐AC) in 289 mOsm, induced a small but significant hyperpolarization of −2.6 mV. Increasing medium osmolality to 344 mOsm enlarged this hyperpolarization significantly to −7.6 mV.
In a solution of 344 mOsm containing 100 μm ouabain, the bumetanide‐induced hyperpolarization of Vm was absent.
The results indicate that a Na‐K‐2Cl cotransporter is present in mouse lumbrical muscle fibre and that its contribution to Vm is dependent on medium osmolality.
British Journal of Pharmacology (1997) 120, 39–44; doi:10.1038/sj.bjp.0700887</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0700887</identifier><identifier>PMID: 9117096</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Biological and medical sciences ; Bumetanide ; Bumetanide - pharmacology ; Carrier Proteins - metabolism ; Chloride Channels - drug effects ; Chloride Channels - metabolism ; Culture Media ; Diuretics - pharmacology ; Female ; Fundamental and applied biological sciences. Psychology ; furosemide ; Furosemide - pharmacology ; In Vitro Techniques ; Kinetics ; Male ; membrane potential ; Membrane Potentials - drug effects ; Mice ; Muscle, Skeletal - drug effects ; Muscle, Skeletal - metabolism ; Na‐K‐2Cl cotransporter ; Osmolar Concentration ; osmoregulation ; ouabain, Na/K‐pump, skeletal muscle ; Potassium - metabolism ; Sodium - metabolism ; Sodium-Potassium-Chloride Symporters ; Sodium-Potassium-Exchanging ATPase - drug effects ; Striated muscle. Tendons ; Vertebrates: osteoarticular system, musculoskeletal system</subject><ispartof>British journal of pharmacology, 1997-01, Vol.120 (1), p.39-44</ispartof><rights>1996 British Pharmacological Society</rights><rights>1997 INIST-CNRS</rights><rights>Copyright 1997, Nature Publishing Group 1997 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5248-e192ae9a40fa22a196b96412f8f18d52fbee968b2c9f16d03abde34d36ef91093</citedby><cites>FETCH-LOGICAL-c5248-e192ae9a40fa22a196b96412f8f18d52fbee968b2c9f16d03abde34d36ef91093</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1564355/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1564355/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,1418,1434,27929,27930,45579,45580,46414,46838,53796,53798</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2557371$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9117096$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Van Mil, H G J</creatorcontrib><creatorcontrib>Geukes Foppen, R J</creatorcontrib><creatorcontrib>Siegenbeek van Heukelom, J</creatorcontrib><title>The influence of bumetanide on the membrane potential of mouse skeletal muscle cells in isotonic and hypertonic media</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Increasing the medium osmolality, with a non‐ionic osmoticant, from control (289 mOsm) to 319 mOsm or 344 mOsm in the lumbrical muscle cell of the mouse, resulted in a depolarization of the membrane potential (Vm) of 5.9 mV and 10.9 mV, respectively.
In control medium, the blockers of chloride related cotransport bumetanide and furosemide, induced a hyperpolarization of −3.6 and −3.0 mV and prevented the depolarization due to hypertonicity. When bumetanide was added in hypertonic media Vm fully repolarized to control values.
In a medium of 266 mOsm, the hyperpolarization by bumetanide was absent.
At 344 mOsm the half‐maximal effective concentration (IC50) was 0.5 μm for bumetanide and 21 μm for furosemide.
In solutions containing 1.25 mm sodium the depolarization by hypertonicity was reduced to 2.3 mV.
Reducing chloride permeability, by anthracene 9 carboxylic acid (9‐AC) in 289 mOsm, induced a small but significant hyperpolarization of −2.6 mV. Increasing medium osmolality to 344 mOsm enlarged this hyperpolarization significantly to −7.6 mV.
In a solution of 344 mOsm containing 100 μm ouabain, the bumetanide‐induced hyperpolarization of Vm was absent.
The results indicate that a Na‐K‐2Cl cotransporter is present in mouse lumbrical muscle fibre and that its contribution to Vm is dependent on medium osmolality.
British Journal of Pharmacology (1997) 120, 39–44; doi:10.1038/sj.bjp.0700887</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bumetanide</subject><subject>Bumetanide - pharmacology</subject><subject>Carrier Proteins - metabolism</subject><subject>Chloride Channels - drug effects</subject><subject>Chloride Channels - metabolism</subject><subject>Culture Media</subject><subject>Diuretics - pharmacology</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>furosemide</subject><subject>Furosemide - pharmacology</subject><subject>In Vitro Techniques</subject><subject>Kinetics</subject><subject>Male</subject><subject>membrane potential</subject><subject>Membrane Potentials - drug effects</subject><subject>Mice</subject><subject>Muscle, Skeletal - drug effects</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Na‐K‐2Cl cotransporter</subject><subject>Osmolar Concentration</subject><subject>osmoregulation</subject><subject>ouabain, Na/K‐pump, skeletal muscle</subject><subject>Potassium - metabolism</subject><subject>Sodium - metabolism</subject><subject>Sodium-Potassium-Chloride Symporters</subject><subject>Sodium-Potassium-Exchanging ATPase - drug effects</subject><subject>Striated muscle. Tendons</subject><subject>Vertebrates: osteoarticular system, musculoskeletal system</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtv1DAUhS1EVYbClh2SF4hdpr5xHNsbJFoBRapEF-3acpxrxoPzIE5A8-_xaKIRrFhZV-fzuY9DyBtgW2BcXaf9ttmPWyYZU0o-IxuoZF0IruA52TDGZAGg1AvyMqU9Y1mU4pJcagDJdL0hy-MOaeh9XLB3SAdPm6XD2fahzVVP5yx32DWT7ZGOw4z9HGw8ct2wJKTpB8aMR9otyUWkDmNM2ZCGNMxDHxy1fUt3hxGnU9lhG-wrcuFtTPh6fa_I0-dPj7d3xf23L19vP94XTpSVKhB0aVHbinlblhZ03ei6gtIrD6oVpW8Qda2a0mkPdcu4bVrkVctr9BqY5lfkw8l3XJrc2OXpJxvNOIXOTgcz2GD-VfqwM9-HXwZEXXEhssH71WAafi6YZtOFdNwxnyPvb6RSwEquMrg9gW4aUprQn5sAM8egTNqbHJRZg8of3v492hlfk8n6u1W3ydnocwAupDNWCiG5hIzxE_Y7RDz8p6m5ebgTIBX_A3Epr_E</recordid><startdate>199701</startdate><enddate>199701</enddate><creator>Van Mil, H G J</creator><creator>Geukes Foppen, R J</creator><creator>Siegenbeek van Heukelom, J</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>199701</creationdate><title>The influence of bumetanide on the membrane potential of mouse skeletal muscle cells in isotonic and hypertonic media</title><author>Van Mil, H G J ; Geukes Foppen, R J ; Siegenbeek van Heukelom, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5248-e192ae9a40fa22a196b96412f8f18d52fbee968b2c9f16d03abde34d36ef91093</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bumetanide</topic><topic>Bumetanide - pharmacology</topic><topic>Carrier Proteins - metabolism</topic><topic>Chloride Channels - drug effects</topic><topic>Chloride Channels - metabolism</topic><topic>Culture Media</topic><topic>Diuretics - pharmacology</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>furosemide</topic><topic>Furosemide - pharmacology</topic><topic>In Vitro Techniques</topic><topic>Kinetics</topic><topic>Male</topic><topic>membrane potential</topic><topic>Membrane Potentials - drug effects</topic><topic>Mice</topic><topic>Muscle, Skeletal - drug effects</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Na‐K‐2Cl cotransporter</topic><topic>Osmolar Concentration</topic><topic>osmoregulation</topic><topic>ouabain, Na/K‐pump, skeletal muscle</topic><topic>Potassium - metabolism</topic><topic>Sodium - metabolism</topic><topic>Sodium-Potassium-Chloride Symporters</topic><topic>Sodium-Potassium-Exchanging ATPase - drug effects</topic><topic>Striated muscle. Tendons</topic><topic>Vertebrates: osteoarticular system, musculoskeletal system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Van Mil, H G J</creatorcontrib><creatorcontrib>Geukes Foppen, R J</creatorcontrib><creatorcontrib>Siegenbeek van Heukelom, J</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Van Mil, H G J</au><au>Geukes Foppen, R J</au><au>Siegenbeek van Heukelom, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The influence of bumetanide on the membrane potential of mouse skeletal muscle cells in isotonic and hypertonic media</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>1997-01</date><risdate>1997</risdate><volume>120</volume><issue>1</issue><spage>39</spage><epage>44</epage><pages>39-44</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Increasing the medium osmolality, with a non‐ionic osmoticant, from control (289 mOsm) to 319 mOsm or 344 mOsm in the lumbrical muscle cell of the mouse, resulted in a depolarization of the membrane potential (Vm) of 5.9 mV and 10.9 mV, respectively.
In control medium, the blockers of chloride related cotransport bumetanide and furosemide, induced a hyperpolarization of −3.6 and −3.0 mV and prevented the depolarization due to hypertonicity. When bumetanide was added in hypertonic media Vm fully repolarized to control values.
In a medium of 266 mOsm, the hyperpolarization by bumetanide was absent.
At 344 mOsm the half‐maximal effective concentration (IC50) was 0.5 μm for bumetanide and 21 μm for furosemide.
In solutions containing 1.25 mm sodium the depolarization by hypertonicity was reduced to 2.3 mV.
Reducing chloride permeability, by anthracene 9 carboxylic acid (9‐AC) in 289 mOsm, induced a small but significant hyperpolarization of −2.6 mV. Increasing medium osmolality to 344 mOsm enlarged this hyperpolarization significantly to −7.6 mV.
In a solution of 344 mOsm containing 100 μm ouabain, the bumetanide‐induced hyperpolarization of Vm was absent.
The results indicate that a Na‐K‐2Cl cotransporter is present in mouse lumbrical muscle fibre and that its contribution to Vm is dependent on medium osmolality.
British Journal of Pharmacology (1997) 120, 39–44; doi:10.1038/sj.bjp.0700887</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>9117096</pmid><doi>10.1038/sj.bjp.0700887</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Bumetanide Bumetanide - pharmacology Carrier Proteins - metabolism Chloride Channels - drug effects Chloride Channels - metabolism Culture Media Diuretics - pharmacology Female Fundamental and applied biological sciences. Psychology furosemide Furosemide - pharmacology In Vitro Techniques Kinetics Male membrane potential Membrane Potentials - drug effects Mice Muscle, Skeletal - drug effects Muscle, Skeletal - metabolism Na‐K‐2Cl cotransporter Osmolar Concentration osmoregulation ouabain, Na/K‐pump, skeletal muscle Potassium - metabolism Sodium - metabolism Sodium-Potassium-Chloride Symporters Sodium-Potassium-Exchanging ATPase - drug effects Striated muscle. Tendons Vertebrates: osteoarticular system, musculoskeletal system |
| title | The influence of bumetanide on the membrane potential of mouse skeletal muscle cells in isotonic and hypertonic media |
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