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
Hauptverfasser: Wong, K. R, Berry, C. A, Cogan, M. G
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container_end_page F729
container_issue 4
container_start_page 723
container_title American journal of physiology. Renal physiology
container_volume 268
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
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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 &lt; 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 &lt; 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 &lt; 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. 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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 &lt; 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 &lt; 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 &lt; 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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ispartof American journal of physiology. Renal physiology, 1995-04, Vol.268 (4), p.723-F729
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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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