Chloride transport in the rat S1 proximal tubule
K. R. Wong, C. A. Berry and M. G. Cogan Department of Medicine, University of California, San Francisco, USA. In vivo microperfusion was used to elucidate the modes and regulation of the powerful chloride transport system resident in the rat early (S1) proximal convoluted tubule (PCT). From a comple...
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Veröffentlicht in: | American journal of physiology. Renal physiology 1995-04, Vol.268 (4), p.723-F729 |
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container_title | American journal of physiology. Renal physiology |
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creator | Wong, K. R Berry, C. A Cogan, M. G |
description | K. R. Wong, C. A. Berry and M. G. Cogan
Department of Medicine, University of California, San Francisco, USA.
In vivo microperfusion was used to elucidate the modes and regulation of
the powerful chloride transport system resident in the rat early (S1)
proximal convoluted tubule (PCT). From a complete, glomerular
ultrafiltrate-like perfusate, omission of organic solutes reduced chloride
absorption by 93 peq.mm-1.min-1 (302 +/- 10 to 209 +/- 24, P < 0.001).
From a high-chloride perfusate (a relatively pure NaCl solution devoid of
bicarbonate and organic solutes), luminal addition of the active transport
inhibitor cyanide reduced chloride absorption by 153 peq.mm-1.min-1 (632
+/- 17 to 479 +/- 9, P < 0.001). Active transport was also estimated
directly as 121 +/- 4 peq.mm-1.min-1 using a solution in which sodium
isethionate isosmotically replaced bicarbonate and organic solutes,
preventing development of a chloride gradient. Intravenous angiotensin II
caused a stimulation of chloride absorption from a high-chloride perfusate
by 55 peq.mm-1.min-1 (632 +/- 17 to 687 +/- 14, P < 0.05), which was
partially cyanide-sensitive (510 +/- 6 peq.mm-1.min-1). In conclusion, the
components of the normal S1 PCT chloride reabsorption (approximately 300
peq.mm-1.min-1) from the glomerular ultrafiltrate consist of the following:
active transport (40-50%), which can be regulated by angiotensin II;
sodium-coupled organic solute transport (30%); and passive, chloride
concentration gradient-driven transport (20-25%). |
doi_str_mv | 10.1152/ajprenal.1995.268.4.F723 |
format | Article |
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Department of Medicine, University of California, San Francisco, USA.
In vivo microperfusion was used to elucidate the modes and regulation of
the powerful chloride transport system resident in the rat early (S1)
proximal convoluted tubule (PCT). From a complete, glomerular
ultrafiltrate-like perfusate, omission of organic solutes reduced chloride
absorption by 93 peq.mm-1.min-1 (302 +/- 10 to 209 +/- 24, P < 0.001).
From a high-chloride perfusate (a relatively pure NaCl solution devoid of
bicarbonate and organic solutes), luminal addition of the active transport
inhibitor cyanide reduced chloride absorption by 153 peq.mm-1.min-1 (632
+/- 17 to 479 +/- 9, P < 0.001). Active transport was also estimated
directly as 121 +/- 4 peq.mm-1.min-1 using a solution in which sodium
isethionate isosmotically replaced bicarbonate and organic solutes,
preventing development of a chloride gradient. Intravenous angiotensin II
caused a stimulation of chloride absorption from a high-chloride perfusate
by 55 peq.mm-1.min-1 (632 +/- 17 to 687 +/- 14, P < 0.05), which was
partially cyanide-sensitive (510 +/- 6 peq.mm-1.min-1). In conclusion, the
components of the normal S1 PCT chloride reabsorption (approximately 300
peq.mm-1.min-1) from the glomerular ultrafiltrate consist of the following:
active transport (40-50%), which can be regulated by angiotensin II;
sodium-coupled organic solute transport (30%); and passive, chloride
concentration gradient-driven transport (20-25%).</description><identifier>ISSN: 0363-6127</identifier><identifier>ISSN: 0002-9513</identifier><identifier>ISSN: 1931-857X</identifier><identifier>EISSN: 2161-1157</identifier><identifier>EISSN: 1522-1466</identifier><identifier>DOI: 10.1152/ajprenal.1995.268.4.F723</identifier><identifier>PMID: 7733330</identifier><language>eng</language><publisher>United States</publisher><subject>Absorption ; Angiotensin II - pharmacology ; Animals ; Biological Transport - drug effects ; Biological Transport, Active ; Chlorides - metabolism ; Kidney Tubules, Proximal - metabolism ; Male ; Osmosis ; Perfusion ; Rats ; Rats, Inbred Strains</subject><ispartof>American journal of physiology. Renal physiology, 1995-04, Vol.268 (4), p.723-F729</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c349t-5fb3333e7b00874e210c921c8ce2b90df16294080586579d34a783919fe1f8223</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7733330$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wong, K. R</creatorcontrib><creatorcontrib>Berry, C. A</creatorcontrib><creatorcontrib>Cogan, M. G</creatorcontrib><title>Chloride transport in the rat S1 proximal tubule</title><title>American journal of physiology. Renal physiology</title><addtitle>Am J Physiol</addtitle><description>K. R. Wong, C. A. Berry and M. G. Cogan
Department of Medicine, University of California, San Francisco, USA.
In vivo microperfusion was used to elucidate the modes and regulation of
the powerful chloride transport system resident in the rat early (S1)
proximal convoluted tubule (PCT). From a complete, glomerular
ultrafiltrate-like perfusate, omission of organic solutes reduced chloride
absorption by 93 peq.mm-1.min-1 (302 +/- 10 to 209 +/- 24, P < 0.001).
From a high-chloride perfusate (a relatively pure NaCl solution devoid of
bicarbonate and organic solutes), luminal addition of the active transport
inhibitor cyanide reduced chloride absorption by 153 peq.mm-1.min-1 (632
+/- 17 to 479 +/- 9, P < 0.001). Active transport was also estimated
directly as 121 +/- 4 peq.mm-1.min-1 using a solution in which sodium
isethionate isosmotically replaced bicarbonate and organic solutes,
preventing development of a chloride gradient. Intravenous angiotensin II
caused a stimulation of chloride absorption from a high-chloride perfusate
by 55 peq.mm-1.min-1 (632 +/- 17 to 687 +/- 14, P < 0.05), which was
partially cyanide-sensitive (510 +/- 6 peq.mm-1.min-1). In conclusion, the
components of the normal S1 PCT chloride reabsorption (approximately 300
peq.mm-1.min-1) from the glomerular ultrafiltrate consist of the following:
active transport (40-50%), which can be regulated by angiotensin II;
sodium-coupled organic solute transport (30%); and passive, chloride
concentration gradient-driven transport (20-25%).</description><subject>Absorption</subject><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Biological Transport - drug effects</subject><subject>Biological Transport, Active</subject><subject>Chlorides - metabolism</subject><subject>Kidney Tubules, Proximal - metabolism</subject><subject>Male</subject><subject>Osmosis</subject><subject>Perfusion</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><issn>0363-6127</issn><issn>0002-9513</issn><issn>1931-857X</issn><issn>2161-1157</issn><issn>1522-1466</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkMtOwzAQRS0EKqXwCUhesUvwI4ntJapoQarEAlhbTjJpUrlJsBNB_x5XKY_ZzGLu3DtzEMKUxJSm7N7segetsTFVKo1ZJuMkXgnGz9Cc0YxGQSTO0ZzwjEcZZeISXXm_I4QFaTZDMyF4KDJHZFnbzjUl4MGZ1vedG3DT4qEG7MyAXynuXffV7I3Fw5iPFq7RRWWsh5tTX6D31ePb8inavKyflw-bqOCJGqK0yo8JIHJCpEiAUVIoRgtZAMsVKSuaMZUQSVKZpUKVPDFCckVVBbSSjPEFupt8Q_7HCH7Q-8YXYK1poRu9FoIlPHwchHISFq7z3kGlexfudQdNiT7C0j-w9BGWDgR0olfT6u0pY8z3UP4unuiEeTzN62ZbfzYOdF8ffNPZbnv4c_1n-A1tt3aU</recordid><startdate>19950401</startdate><enddate>19950401</enddate><creator>Wong, K. R</creator><creator>Berry, C. A</creator><creator>Cogan, M. G</creator><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></search><sort><creationdate>19950401</creationdate><title>Chloride transport in the rat S1 proximal tubule</title><author>Wong, K. R ; Berry, C. A ; Cogan, M. G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c349t-5fb3333e7b00874e210c921c8ce2b90df16294080586579d34a783919fe1f8223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Absorption</topic><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Biological Transport - drug effects</topic><topic>Biological Transport, Active</topic><topic>Chlorides - metabolism</topic><topic>Kidney Tubules, Proximal - metabolism</topic><topic>Male</topic><topic>Osmosis</topic><topic>Perfusion</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wong, K. R</creatorcontrib><creatorcontrib>Berry, C. A</creatorcontrib><creatorcontrib>Cogan, M. G</creatorcontrib><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><jtitle>American journal of physiology. Renal physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wong, K. R</au><au>Berry, C. A</au><au>Cogan, M. G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chloride transport in the rat S1 proximal tubule</atitle><jtitle>American journal of physiology. Renal physiology</jtitle><addtitle>Am J Physiol</addtitle><date>1995-04-01</date><risdate>1995</risdate><volume>268</volume><issue>4</issue><spage>723</spage><epage>F729</epage><pages>723-F729</pages><issn>0363-6127</issn><issn>0002-9513</issn><issn>1931-857X</issn><eissn>2161-1157</eissn><eissn>1522-1466</eissn><abstract>K. R. Wong, C. A. Berry and M. G. Cogan
Department of Medicine, University of California, San Francisco, USA.
In vivo microperfusion was used to elucidate the modes and regulation of
the powerful chloride transport system resident in the rat early (S1)
proximal convoluted tubule (PCT). From a complete, glomerular
ultrafiltrate-like perfusate, omission of organic solutes reduced chloride
absorption by 93 peq.mm-1.min-1 (302 +/- 10 to 209 +/- 24, P < 0.001).
From a high-chloride perfusate (a relatively pure NaCl solution devoid of
bicarbonate and organic solutes), luminal addition of the active transport
inhibitor cyanide reduced chloride absorption by 153 peq.mm-1.min-1 (632
+/- 17 to 479 +/- 9, P < 0.001). Active transport was also estimated
directly as 121 +/- 4 peq.mm-1.min-1 using a solution in which sodium
isethionate isosmotically replaced bicarbonate and organic solutes,
preventing development of a chloride gradient. Intravenous angiotensin II
caused a stimulation of chloride absorption from a high-chloride perfusate
by 55 peq.mm-1.min-1 (632 +/- 17 to 687 +/- 14, P < 0.05), which was
partially cyanide-sensitive (510 +/- 6 peq.mm-1.min-1). In conclusion, the
components of the normal S1 PCT chloride reabsorption (approximately 300
peq.mm-1.min-1) from the glomerular ultrafiltrate consist of the following:
active transport (40-50%), which can be regulated by angiotensin II;
sodium-coupled organic solute transport (30%); and passive, chloride
concentration gradient-driven transport (20-25%).</abstract><cop>United States</cop><pmid>7733330</pmid><doi>10.1152/ajprenal.1995.268.4.F723</doi></addata></record> |
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language | eng |
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source | MEDLINE; Alma/SFX Local Collection |
subjects | Absorption Angiotensin II - pharmacology Animals Biological Transport - drug effects Biological Transport, Active Chlorides - metabolism Kidney Tubules, Proximal - metabolism Male Osmosis Perfusion Rats Rats, Inbred Strains |
title | Chloride transport in the rat S1 proximal tubule |
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