Active transport of the angiotensin‐II antagonist losartan and its main metabolite EXP 3174 across MDCK‐MDR1 and Caco‐2 cell monolayers
We studied the functional interaction between transport and metabolism by comparing the transport of losartan and its active metabolite EXP 3174 (EXP) across cell monolayers. Epithelial layers of Caco‐2 cells as well as MDR1, MRP‐1 and MRP‐2 overexpressing cells, in comparison to the respective wild...
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| Veröffentlicht in: | British journal of pharmacology 2000-03, Vol.129 (6), p.1235-1243 |
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| creator | Soldner, Andrea Benet, Leslie Z Mutschler, Ernst Christians, Uwe |
| description | We studied the functional interaction between transport and metabolism by comparing the transport of losartan and its active metabolite EXP 3174 (EXP) across cell monolayers.
Epithelial layers of Caco‐2 cells as well as MDR1, MRP‐1 and MRP‐2 overexpressing cells, in comparison to the respective wildtypes, were used to characterize the transcellular transport of losartan and EXP.
Losartan transport in MDCK‐MDR1 and Caco‐2 cells was saturable and energy‐dependent with a significantly greater basolateral‐to‐apical (B/A) than apical‐to‐basolateral (A/B) flux (ratio=31±1 in MDCK‐MDR1 and ratio 4±1 in Caco‐2 cells). The B/A flux of losartan was inhibited by cyclosporine and vinblastine, inhibitors of P‐glycoprotein and MRP. In contrast, no active losartan transport was observed in MRP‐1 or MRP‐2 overexpressing cells.
The metabolite was only transported in Caco‐2 cells with a B/A‐to‐A/B ratio of 5±1, while lacking active transport in the MDR1, MRP‐1 or MRP‐2 overexpressing cells. The B/A flux of EXP was significantly inhibited by cyclosporine and vinblastine.
In conclusion, losartan is transported by P‐glycoprotein and other intestinal transporters, that do not include MRP‐1 and MRP‐2. In contrast, the carboxylic acid metabolite is not a P‐glycoprotein substrate, but displays considerably higher affinity for other transporters than losartan, that again most probably do not include MRP‐1 and MRP‐2.
British Journal of Pharmacology (2000) 129, 1235–1243; doi:10.1038/sj.bjp.0703150 |
| doi_str_mv | 10.1038/sj.bjp.0703150 |
| format | Article |
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Epithelial layers of Caco‐2 cells as well as MDR1, MRP‐1 and MRP‐2 overexpressing cells, in comparison to the respective wildtypes, were used to characterize the transcellular transport of losartan and EXP.
Losartan transport in MDCK‐MDR1 and Caco‐2 cells was saturable and energy‐dependent with a significantly greater basolateral‐to‐apical (B/A) than apical‐to‐basolateral (A/B) flux (ratio=31±1 in MDCK‐MDR1 and ratio 4±1 in Caco‐2 cells). The B/A flux of losartan was inhibited by cyclosporine and vinblastine, inhibitors of P‐glycoprotein and MRP. In contrast, no active losartan transport was observed in MRP‐1 or MRP‐2 overexpressing cells.
The metabolite was only transported in Caco‐2 cells with a B/A‐to‐A/B ratio of 5±1, while lacking active transport in the MDR1, MRP‐1 or MRP‐2 overexpressing cells. The B/A flux of EXP was significantly inhibited by cyclosporine and vinblastine.
In conclusion, losartan is transported by P‐glycoprotein and other intestinal transporters, that do not include MRP‐1 and MRP‐2. In contrast, the carboxylic acid metabolite is not a P‐glycoprotein substrate, but displays considerably higher affinity for other transporters than losartan, that again most probably do not include MRP‐1 and MRP‐2.
British Journal of Pharmacology (2000) 129, 1235–1243; doi:10.1038/sj.bjp.0703150</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0703150</identifier><identifier>PMID: 10725273</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>2,4-Dinitrophenol - pharmacology ; Angiotensin II - antagonists & inhibitors ; Angiotensin‐II antagonists ; Animals ; Anti-Arrhythmia Agents - metabolism ; Antihypertensive agents ; Antimetabolites - pharmacology ; Biological and medical sciences ; Biological Transport, Active - drug effects ; Caco-2 Cells ; Cardiovascular system ; Cell Line ; Cell physiology ; Chromatography, Liquid ; Dogs ; Energy Metabolism - drug effects ; Energy Metabolism - physiology ; Epithelium - drug effects ; Epithelium - metabolism ; Fundamental and applied biological sciences. Psychology ; Humans ; Imidazoles - metabolism ; intestinal drug transporters ; Kidney - drug effects ; Kidney - metabolism ; Kinetics ; LLC-PK1 Cells ; Losartan - metabolism ; Mass Spectrometry ; MDCK‐MDR1 cells ; Medical sciences ; Membrane and intracellular transports ; Molecular and cellular biology ; Pharmacology. Drug treatments ; P‐glycoprotein ; Swine ; Temperature ; Tetrazoles - metabolism</subject><ispartof>British journal of pharmacology, 2000-03, Vol.129 (6), p.1235-1243</ispartof><rights>2000 British Pharmacological Society</rights><rights>2000 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Mar 2000</rights><rights>Copyright 2000, Nature Publishing Group 2000 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5858-a32934b6260a21de38b39f0182ac601abddce7b7becd5633fd90ff82348023fd3</citedby><cites>FETCH-LOGICAL-c5858-a32934b6260a21de38b39f0182ac601abddce7b7becd5633fd90ff82348023fd3</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/PMC1571937/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1571937/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27903,27904,45553,45554,46387,46811,53769,53771</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1297216$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10725273$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Soldner, Andrea</creatorcontrib><creatorcontrib>Benet, Leslie Z</creatorcontrib><creatorcontrib>Mutschler, Ernst</creatorcontrib><creatorcontrib>Christians, Uwe</creatorcontrib><title>Active transport of the angiotensin‐II antagonist losartan and its main metabolite EXP 3174 across MDCK‐MDR1 and Caco‐2 cell monolayers</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>We studied the functional interaction between transport and metabolism by comparing the transport of losartan and its active metabolite EXP 3174 (EXP) across cell monolayers.
Epithelial layers of Caco‐2 cells as well as MDR1, MRP‐1 and MRP‐2 overexpressing cells, in comparison to the respective wildtypes, were used to characterize the transcellular transport of losartan and EXP.
Losartan transport in MDCK‐MDR1 and Caco‐2 cells was saturable and energy‐dependent with a significantly greater basolateral‐to‐apical (B/A) than apical‐to‐basolateral (A/B) flux (ratio=31±1 in MDCK‐MDR1 and ratio 4±1 in Caco‐2 cells). The B/A flux of losartan was inhibited by cyclosporine and vinblastine, inhibitors of P‐glycoprotein and MRP. In contrast, no active losartan transport was observed in MRP‐1 or MRP‐2 overexpressing cells.
The metabolite was only transported in Caco‐2 cells with a B/A‐to‐A/B ratio of 5±1, while lacking active transport in the MDR1, MRP‐1 or MRP‐2 overexpressing cells. The B/A flux of EXP was significantly inhibited by cyclosporine and vinblastine.
In conclusion, losartan is transported by P‐glycoprotein and other intestinal transporters, that do not include MRP‐1 and MRP‐2. In contrast, the carboxylic acid metabolite is not a P‐glycoprotein substrate, but displays considerably higher affinity for other transporters than losartan, that again most probably do not include MRP‐1 and MRP‐2.
British Journal of Pharmacology (2000) 129, 1235–1243; doi:10.1038/sj.bjp.0703150</description><subject>2,4-Dinitrophenol - pharmacology</subject><subject>Angiotensin II - antagonists & inhibitors</subject><subject>Angiotensin‐II antagonists</subject><subject>Animals</subject><subject>Anti-Arrhythmia Agents - metabolism</subject><subject>Antihypertensive agents</subject><subject>Antimetabolites - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Biological Transport, Active - drug effects</subject><subject>Caco-2 Cells</subject><subject>Cardiovascular system</subject><subject>Cell Line</subject><subject>Cell physiology</subject><subject>Chromatography, Liquid</subject><subject>Dogs</subject><subject>Energy Metabolism - drug effects</subject><subject>Energy Metabolism - physiology</subject><subject>Epithelium - drug effects</subject><subject>Epithelium - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Humans</subject><subject>Imidazoles - metabolism</subject><subject>intestinal drug transporters</subject><subject>Kidney - drug effects</subject><subject>Kidney - metabolism</subject><subject>Kinetics</subject><subject>LLC-PK1 Cells</subject><subject>Losartan - metabolism</subject><subject>Mass Spectrometry</subject><subject>MDCK‐MDR1 cells</subject><subject>Medical sciences</subject><subject>Membrane and intracellular transports</subject><subject>Molecular and cellular biology</subject><subject>Pharmacology. Drug treatments</subject><subject>P‐glycoprotein</subject><subject>Swine</subject><subject>Temperature</subject><subject>Tetrazoles - metabolism</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkcFuEzEQhlcIREPhyhFZiAOXDR47u3YuSCUtNKIVFQKJmzXr9aZe7dqp7RTlxgsg8Yw8CW4TQeHCyRrPN7_9z18UT4FOgXL5KvbTpl9PqaAcKnqvmMBM1GXFJdwvJpRSUQJIeVA8irGnNDdF9bA4ACpYxQSfFN-PdLLXhqSALq59SMR3JF0agm5lfTIuWvfz24_lMl8kXHlnYyKDjxgSunzXEpsiGdE6MpqEjR9sMuTkywXhIGYEdfAxkvPjxfuscn78EW5nFqh9rhnRZhjI6J0fcGtCfFw86HCI5sn-PCw-vz35tDgtzz68Wy6OzkpdyUqWyNmcz5qa1RQZtIbLhs87CpKhrilg07baiEY0RrdVzXnXzmnXScZnkrJc8cPi9U53vWlGk2GX_Q9qHeyIYas8WvV3x9lLtfLXCioBcy6ywMu9QPBXGxOTGm28MYPO-E1UIDOU9y1lRp__g_Z-E1y2pxgIkFRSyNB0B93uK5ju91-AqpugVexVDlrtg84Dz-46uIPvks3Aiz2AUePQ5Xy1jX84NhcM6ozxHfbVDmb7n1fVm4tTXleS_wIYLsUA</recordid><startdate>200003</startdate><enddate>200003</enddate><creator>Soldner, Andrea</creator><creator>Benet, Leslie Z</creator><creator>Mutschler, Ernst</creator><creator>Christians, Uwe</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7U7</scope><scope>C1K</scope><scope>5PM</scope></search><sort><creationdate>200003</creationdate><title>Active transport of the angiotensin‐II antagonist losartan and its main metabolite EXP 3174 across MDCK‐MDR1 and Caco‐2 cell monolayers</title><author>Soldner, Andrea ; Benet, Leslie Z ; Mutschler, Ernst ; Christians, Uwe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5858-a32934b6260a21de38b39f0182ac601abddce7b7becd5633fd90ff82348023fd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>2,4-Dinitrophenol - pharmacology</topic><topic>Angiotensin II - antagonists & inhibitors</topic><topic>Angiotensin‐II antagonists</topic><topic>Animals</topic><topic>Anti-Arrhythmia Agents - metabolism</topic><topic>Antihypertensive agents</topic><topic>Antimetabolites - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Biological Transport, Active - drug effects</topic><topic>Caco-2 Cells</topic><topic>Cardiovascular system</topic><topic>Cell Line</topic><topic>Cell physiology</topic><topic>Chromatography, Liquid</topic><topic>Dogs</topic><topic>Energy Metabolism - drug effects</topic><topic>Energy Metabolism - physiology</topic><topic>Epithelium - drug effects</topic><topic>Epithelium - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Humans</topic><topic>Imidazoles - metabolism</topic><topic>intestinal drug transporters</topic><topic>Kidney - drug effects</topic><topic>Kidney - metabolism</topic><topic>Kinetics</topic><topic>LLC-PK1 Cells</topic><topic>Losartan - metabolism</topic><topic>Mass Spectrometry</topic><topic>MDCK‐MDR1 cells</topic><topic>Medical sciences</topic><topic>Membrane and intracellular transports</topic><topic>Molecular and cellular biology</topic><topic>Pharmacology. Drug treatments</topic><topic>P‐glycoprotein</topic><topic>Swine</topic><topic>Temperature</topic><topic>Tetrazoles - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Soldner, Andrea</creatorcontrib><creatorcontrib>Benet, Leslie Z</creatorcontrib><creatorcontrib>Mutschler, Ernst</creatorcontrib><creatorcontrib>Christians, Uwe</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>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</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>Soldner, Andrea</au><au>Benet, Leslie Z</au><au>Mutschler, Ernst</au><au>Christians, Uwe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Active transport of the angiotensin‐II antagonist losartan and its main metabolite EXP 3174 across MDCK‐MDR1 and Caco‐2 cell monolayers</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2000-03</date><risdate>2000</risdate><volume>129</volume><issue>6</issue><spage>1235</spage><epage>1243</epage><pages>1235-1243</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>We studied the functional interaction between transport and metabolism by comparing the transport of losartan and its active metabolite EXP 3174 (EXP) across cell monolayers.
Epithelial layers of Caco‐2 cells as well as MDR1, MRP‐1 and MRP‐2 overexpressing cells, in comparison to the respective wildtypes, were used to characterize the transcellular transport of losartan and EXP.
Losartan transport in MDCK‐MDR1 and Caco‐2 cells was saturable and energy‐dependent with a significantly greater basolateral‐to‐apical (B/A) than apical‐to‐basolateral (A/B) flux (ratio=31±1 in MDCK‐MDR1 and ratio 4±1 in Caco‐2 cells). The B/A flux of losartan was inhibited by cyclosporine and vinblastine, inhibitors of P‐glycoprotein and MRP. In contrast, no active losartan transport was observed in MRP‐1 or MRP‐2 overexpressing cells.
The metabolite was only transported in Caco‐2 cells with a B/A‐to‐A/B ratio of 5±1, while lacking active transport in the MDR1, MRP‐1 or MRP‐2 overexpressing cells. The B/A flux of EXP was significantly inhibited by cyclosporine and vinblastine.
In conclusion, losartan is transported by P‐glycoprotein and other intestinal transporters, that do not include MRP‐1 and MRP‐2. In contrast, the carboxylic acid metabolite is not a P‐glycoprotein substrate, but displays considerably higher affinity for other transporters than losartan, that again most probably do not include MRP‐1 and MRP‐2.
British Journal of Pharmacology (2000) 129, 1235–1243; doi:10.1038/sj.bjp.0703150</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>10725273</pmid><doi>10.1038/sj.bjp.0703150</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | British journal of pharmacology, 2000-03, Vol.129 (6), p.1235-1243 |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Wiley Free Content; PubMed Central; Alma/SFX Local Collection |
| subjects | 2,4-Dinitrophenol - pharmacology Angiotensin II - antagonists & inhibitors Angiotensin‐II antagonists Animals Anti-Arrhythmia Agents - metabolism Antihypertensive agents Antimetabolites - pharmacology Biological and medical sciences Biological Transport, Active - drug effects Caco-2 Cells Cardiovascular system Cell Line Cell physiology Chromatography, Liquid Dogs Energy Metabolism - drug effects Energy Metabolism - physiology Epithelium - drug effects Epithelium - metabolism Fundamental and applied biological sciences. Psychology Humans Imidazoles - metabolism intestinal drug transporters Kidney - drug effects Kidney - metabolism Kinetics LLC-PK1 Cells Losartan - metabolism Mass Spectrometry MDCK‐MDR1 cells Medical sciences Membrane and intracellular transports Molecular and cellular biology Pharmacology. Drug treatments P‐glycoprotein Swine Temperature Tetrazoles - metabolism |
| title | Active transport of the angiotensin‐II antagonist losartan and its main metabolite EXP 3174 across MDCK‐MDR1 and Caco‐2 cell monolayers |
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