Urinary Potassium Excretion and Sodium Sensitivity in Blacks
ABSTRACT—Based on racial differences in urinary potassium excretion and responses to diuretics, we present a model suggesting that a major cause of sodium sensitivity in blacks is an augmented activity of the Na-K-2Cl cotransport in the thick ascending limb of Henle’s loop. This would result in an i...
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Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2004-04, Vol.43 (4), p.707-713 |
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creator | Aviv, Abraham Hollenberg, Norman K Weder, Alan |
description | ABSTRACT—Based on racial differences in urinary potassium excretion and responses to diuretics, we present a model suggesting that a major cause of sodium sensitivity in blacks is an augmented activity of the Na-K-2Cl cotransport in the thick ascending limb of Henle’s loop. This would result in an increased ability to conserve not only sodium but also water, and an upward and rightward shift in the operating point of tubuloglomerular feedback, which may cause an increase in the glomerular capillary hydraulic pressure and predilection to glomerular injury with and without hypertension. In this sense, the biological implication of sodium sensitivity in blacks and in humans in general has ramifications above and beyond salt-evoked increase in blood pressure. |
doi_str_mv | 10.1161/01.HYP.0000120155.48024.6f |
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This would result in an increased ability to conserve not only sodium but also water, and an upward and rightward shift in the operating point of tubuloglomerular feedback, which may cause an increase in the glomerular capillary hydraulic pressure and predilection to glomerular injury with and without hypertension. In this sense, the biological implication of sodium sensitivity in blacks and in humans in general has ramifications above and beyond salt-evoked increase in blood pressure.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.HYP.0000120155.48024.6f</identifier><identifier>PMID: 14967834</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>African Continental Ancestry Group - genetics ; Animals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Cardiology. Vascular system ; Chlorides - pharmacokinetics ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Disease Models, Animal ; Diuresis - genetics ; Fundamental and applied biological sciences. Psychology ; Genetic Predisposition to Disease ; Humans ; Hypertension - ethnology ; Hypertension - etiology ; Hypertension - genetics ; Hypertension - physiopathology ; Ion Transport - genetics ; Kidney Glomerulus - pathology ; Kidney Glomerulus - physiopathology ; Kidney Tubules - metabolism ; Loop of Henle - metabolism ; Medical sciences ; Models, Biological ; Natriuresis - genetics ; Potassium - pharmacokinetics ; Potassium - urine ; Rats ; Rats, Inbred Dahl ; Selection, Genetic ; Sodium Chloride, Dietary - adverse effects ; Sodium Chloride, Dietary - pharmacokinetics ; Sodium, Dietary - adverse effects ; Sodium, Dietary - pharmacokinetics ; Sodium-Potassium-Chloride Symporters - genetics ; Sodium-Potassium-Chloride Symporters - metabolism ; Vertebrates: urinary system</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2004-04, Vol.43 (4), p.707-713</ispartof><rights>2004 American Heart Association, Inc.</rights><rights>2004 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Apr 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5763-74494157a14e034309ef219a9908a5572fd0a782f621cd8a7bb381c6a5932baf3</citedby><cites>FETCH-LOGICAL-c5763-74494157a14e034309ef219a9908a5572fd0a782f621cd8a7bb381c6a5932baf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3685,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15621888$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14967834$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aviv, Abraham</creatorcontrib><creatorcontrib>Hollenberg, Norman K</creatorcontrib><creatorcontrib>Weder, Alan</creatorcontrib><title>Urinary Potassium Excretion and Sodium Sensitivity in Blacks</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>ABSTRACT—Based on racial differences in urinary potassium excretion and responses to diuretics, we present a model suggesting that a major cause of sodium sensitivity in blacks is an augmented activity of the Na-K-2Cl cotransport in the thick ascending limb of Henle’s loop. This would result in an increased ability to conserve not only sodium but also water, and an upward and rightward shift in the operating point of tubuloglomerular feedback, which may cause an increase in the glomerular capillary hydraulic pressure and predilection to glomerular injury with and without hypertension. In this sense, the biological implication of sodium sensitivity in blacks and in humans in general has ramifications above and beyond salt-evoked increase in blood pressure.</description><subject>African Continental Ancestry Group - genetics</subject><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Chlorides - pharmacokinetics</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Disease Models, Animal</subject><subject>Diuresis - genetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic Predisposition to Disease</subject><subject>Humans</subject><subject>Hypertension - ethnology</subject><subject>Hypertension - etiology</subject><subject>Hypertension - genetics</subject><subject>Hypertension - physiopathology</subject><subject>Ion Transport - genetics</subject><subject>Kidney Glomerulus - pathology</subject><subject>Kidney Glomerulus - physiopathology</subject><subject>Kidney Tubules - metabolism</subject><subject>Loop of Henle - metabolism</subject><subject>Medical sciences</subject><subject>Models, Biological</subject><subject>Natriuresis - genetics</subject><subject>Potassium - pharmacokinetics</subject><subject>Potassium - urine</subject><subject>Rats</subject><subject>Rats, Inbred Dahl</subject><subject>Selection, Genetic</subject><subject>Sodium Chloride, Dietary - adverse effects</subject><subject>Sodium Chloride, Dietary - pharmacokinetics</subject><subject>Sodium, Dietary - adverse effects</subject><subject>Sodium, Dietary - pharmacokinetics</subject><subject>Sodium-Potassium-Chloride Symporters - genetics</subject><subject>Sodium-Potassium-Chloride Symporters - metabolism</subject><subject>Vertebrates: urinary system</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkFFr2zAQx8XoaLKuX2GYQh_t6aSTLI29tKVbBoEVukL7JBRbpmodu5XsZfn2k5NApIeD4yf9736EXAAtACR8pVAsnu4Kmg4wCkIUqCjDQjYfyBwEwxyF5CdkTkFjrgEeZ-RTjC8JR8TylMwAtSwVxzn5_hB8Z8M2u-sHG6Mf19ntvyq4wfddZrs6u-_rqXnvuugH_9cP28x32XVrq9f4mXxsbBvd-aGekYcft39uFvny989fN1fLvBKl5HmJqBFEaQEd5cipdg0DbbWmygpRsqamtlSskQyqWtlyteIKKmmF5mxlG35GLvb_voX-fXRxMC_9GLoUaRgVTHEKKkHf9lAV-hiDa8xb8Ou0mgFqJm-GgknezNGb2Xkzckr4ckgYV2tXH58eRCXg8gDYWNm2CbarfDxyIs2u1DQF7rlN3w4uxNd23Lhgnp1th-ddNDKpcpZqupTmU4vz__4HhEg</recordid><startdate>200404</startdate><enddate>200404</enddate><creator>Aviv, Abraham</creator><creator>Hollenberg, Norman K</creator><creator>Weder, Alan</creator><general>American Heart Association, Inc</general><general>Lippincott</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>K9.</scope></search><sort><creationdate>200404</creationdate><title>Urinary Potassium Excretion and Sodium Sensitivity in Blacks</title><author>Aviv, Abraham ; Hollenberg, Norman K ; Weder, Alan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5763-74494157a14e034309ef219a9908a5572fd0a782f621cd8a7bb381c6a5932baf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>African Continental Ancestry Group - genetics</topic><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Chlorides - pharmacokinetics</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Disease Models, Animal</topic><topic>Diuresis - genetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genetic Predisposition to Disease</topic><topic>Humans</topic><topic>Hypertension - ethnology</topic><topic>Hypertension - etiology</topic><topic>Hypertension - genetics</topic><topic>Hypertension - physiopathology</topic><topic>Ion Transport - genetics</topic><topic>Kidney Glomerulus - pathology</topic><topic>Kidney Glomerulus - physiopathology</topic><topic>Kidney Tubules - metabolism</topic><topic>Loop of Henle - metabolism</topic><topic>Medical sciences</topic><topic>Models, Biological</topic><topic>Natriuresis - genetics</topic><topic>Potassium - pharmacokinetics</topic><topic>Potassium - urine</topic><topic>Rats</topic><topic>Rats, Inbred Dahl</topic><topic>Selection, Genetic</topic><topic>Sodium Chloride, Dietary - adverse effects</topic><topic>Sodium Chloride, Dietary - pharmacokinetics</topic><topic>Sodium, Dietary - adverse effects</topic><topic>Sodium, Dietary - pharmacokinetics</topic><topic>Sodium-Potassium-Chloride Symporters - genetics</topic><topic>Sodium-Potassium-Chloride Symporters - metabolism</topic><topic>Vertebrates: urinary system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aviv, Abraham</creatorcontrib><creatorcontrib>Hollenberg, Norman K</creatorcontrib><creatorcontrib>Weder, Alan</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 Health & Medical Complete (Alumni)</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aviv, Abraham</au><au>Hollenberg, Norman K</au><au>Weder, Alan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Urinary Potassium Excretion and Sodium Sensitivity in Blacks</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2004-04</date><risdate>2004</risdate><volume>43</volume><issue>4</issue><spage>707</spage><epage>713</epage><pages>707-713</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>ABSTRACT—Based on racial differences in urinary potassium excretion and responses to diuretics, we present a model suggesting that a major cause of sodium sensitivity in blacks is an augmented activity of the Na-K-2Cl cotransport in the thick ascending limb of Henle’s loop. This would result in an increased ability to conserve not only sodium but also water, and an upward and rightward shift in the operating point of tubuloglomerular feedback, which may cause an increase in the glomerular capillary hydraulic pressure and predilection to glomerular injury with and without hypertension. In this sense, the biological implication of sodium sensitivity in blacks and in humans in general has ramifications above and beyond salt-evoked increase in blood pressure.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>14967834</pmid><doi>10.1161/01.HYP.0000120155.48024.6f</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
subjects | African Continental Ancestry Group - genetics Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Cardiology. Vascular system Chlorides - pharmacokinetics Clinical manifestations. Epidemiology. Investigative techniques. Etiology Disease Models, Animal Diuresis - genetics Fundamental and applied biological sciences. Psychology Genetic Predisposition to Disease Humans Hypertension - ethnology Hypertension - etiology Hypertension - genetics Hypertension - physiopathology Ion Transport - genetics Kidney Glomerulus - pathology Kidney Glomerulus - physiopathology Kidney Tubules - metabolism Loop of Henle - metabolism Medical sciences Models, Biological Natriuresis - genetics Potassium - pharmacokinetics Potassium - urine Rats Rats, Inbred Dahl Selection, Genetic Sodium Chloride, Dietary - adverse effects Sodium Chloride, Dietary - pharmacokinetics Sodium, Dietary - adverse effects Sodium, Dietary - pharmacokinetics Sodium-Potassium-Chloride Symporters - genetics Sodium-Potassium-Chloride Symporters - metabolism Vertebrates: urinary system |
title | Urinary Potassium Excretion and Sodium Sensitivity in Blacks |
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