Epithelial Sodium Channel and Salt-Sensitive Hypertension

The development of high blood pressure is influenced by genetic and environmental factors, with high salt intake being a known environmental contributor. Humans display a spectrum of sodium-sensitivity, with some individuals displaying a significant blood pressure rise in response to increased sodiu...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2021-03, Vol.77 (3), p.759-767
Hauptverfasser: Mutchler, Stephanie M., Kirabo, Annet, Kleyman, Thomas R.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 767
container_issue 3
container_start_page 759
container_title Hypertension (Dallas, Tex. 1979)
container_volume 77
creator Mutchler, Stephanie M.
Kirabo, Annet
Kleyman, Thomas R.
description The development of high blood pressure is influenced by genetic and environmental factors, with high salt intake being a known environmental contributor. Humans display a spectrum of sodium-sensitivity, with some individuals displaying a significant blood pressure rise in response to increased sodium intake while others experience almost no change. These differences are, in part, attributable to genetic variation in pathways involved in sodium handling and excretion. ENaC (epithelial sodium channel) is one of the key transporters responsible for the reabsorption of sodium in the distal nephron. This channel has an important role in the regulation of extracellular fluid volume and consequently blood pressure. Herein, we review the role of ENaC in the development of salt-sensitive hypertension, and present mechanistic insights into the regulation of ENaC activity and how it may accelerate sodium-induced damage and dysfunction. We discuss the traditional role of ENaC in renal sodium reabsorption and review work addressing ENaC expression and function in the brain, vasculature, and immune cells, and how this has expanded the implications for its role in the initiation and progression of salt-sensitive hypertension.
doi_str_mv 10.1161/HYPERTENSIONAHA.120.14481
format Article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7878349</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2480741628</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5344-7a9b8c9cfa99e77d625643f880a2f194cf9e14f89d72f01df1cf3100137d33d13</originalsourceid><addsrcrecordid>eNpdkE9P3DAQxa2qVVn-fIUqvfUS6rG9sX2ptFotLBICxIIEJ8sk48atN1nsBMS3r2EpavEcLM-8eX76EfIV6CFABd-XtxeLy6vF2erk_Gy2nB0CywMhFHwgE5gyUYppxT-SCQUtSg1ws0N2U_pFaRYJ-ZnscC5UpZWaEL3Y-KHF4G0oVn3jx3Uxb23XYShs1xQrG4ZyhV3yg3_AYvm0wTg8P_tun3xyNiQ8eL33yPXR4mq-LE_Pj0_ms9OynnIhSmn1nap17azWKGVTsWkluFOKWuZyvtppBOGUbiRzFBoHteOQo3LZcN4A3yM_tr6b8W6NTY3dEG0wm-jXNj6Z3nrz_6TzrfnZPxippOJCZ4Nvrwaxvx8xDWbtU40h2A77MRkmFJUCKqayVG-ldexTiujevgFqntGbd-hNRm9e0OfdL__mfNv8yzoLxFbw2IcBY_odxkeMpsXMuDU0H8EqVTLKgPJc5UuL_wE2EJHh</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2480741628</pqid></control><display><type>article</type><title>Epithelial Sodium Channel and Salt-Sensitive Hypertension</title><source>MEDLINE</source><source>American Heart Association Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Mutchler, Stephanie M. ; Kirabo, Annet ; Kleyman, Thomas R.</creator><creatorcontrib>Mutchler, Stephanie M. ; Kirabo, Annet ; Kleyman, Thomas R.</creatorcontrib><description>The development of high blood pressure is influenced by genetic and environmental factors, with high salt intake being a known environmental contributor. Humans display a spectrum of sodium-sensitivity, with some individuals displaying a significant blood pressure rise in response to increased sodium intake while others experience almost no change. These differences are, in part, attributable to genetic variation in pathways involved in sodium handling and excretion. ENaC (epithelial sodium channel) is one of the key transporters responsible for the reabsorption of sodium in the distal nephron. This channel has an important role in the regulation of extracellular fluid volume and consequently blood pressure. Herein, we review the role of ENaC in the development of salt-sensitive hypertension, and present mechanistic insights into the regulation of ENaC activity and how it may accelerate sodium-induced damage and dysfunction. We discuss the traditional role of ENaC in renal sodium reabsorption and review work addressing ENaC expression and function in the brain, vasculature, and immune cells, and how this has expanded the implications for its role in the initiation and progression of salt-sensitive hypertension.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/HYPERTENSIONAHA.120.14481</identifier><identifier>PMID: 33486988</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Animals ; Blood Pressure - physiology ; Epithelial Sodium Channels - metabolism ; Humans ; Hypertension - etiology ; Hypertension - metabolism ; Hypertension - physiopathology ; Ion Transport ; Kidney - metabolism ; Models, Biological ; Nephrons - metabolism ; Sodium Chloride, Dietary - administration &amp; dosage ; Sodium Chloride, Dietary - adverse effects ; Sodium Chloride, Dietary - metabolism</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2021-03, Vol.77 (3), p.759-767</ispartof><rights>American Heart Association, Inc</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5344-7a9b8c9cfa99e77d625643f880a2f194cf9e14f89d72f01df1cf3100137d33d13</citedby><cites>FETCH-LOGICAL-c5344-7a9b8c9cfa99e77d625643f880a2f194cf9e14f89d72f01df1cf3100137d33d13</cites><orcidid>0000-0002-4288-4452 ; 0000-0002-2413-5415 ; 0000-0001-8580-9359</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3687,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33486988$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mutchler, Stephanie M.</creatorcontrib><creatorcontrib>Kirabo, Annet</creatorcontrib><creatorcontrib>Kleyman, Thomas R.</creatorcontrib><title>Epithelial Sodium Channel and Salt-Sensitive Hypertension</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>The development of high blood pressure is influenced by genetic and environmental factors, with high salt intake being a known environmental contributor. Humans display a spectrum of sodium-sensitivity, with some individuals displaying a significant blood pressure rise in response to increased sodium intake while others experience almost no change. These differences are, in part, attributable to genetic variation in pathways involved in sodium handling and excretion. ENaC (epithelial sodium channel) is one of the key transporters responsible for the reabsorption of sodium in the distal nephron. This channel has an important role in the regulation of extracellular fluid volume and consequently blood pressure. Herein, we review the role of ENaC in the development of salt-sensitive hypertension, and present mechanistic insights into the regulation of ENaC activity and how it may accelerate sodium-induced damage and dysfunction. We discuss the traditional role of ENaC in renal sodium reabsorption and review work addressing ENaC expression and function in the brain, vasculature, and immune cells, and how this has expanded the implications for its role in the initiation and progression of salt-sensitive hypertension.</description><subject>Animals</subject><subject>Blood Pressure - physiology</subject><subject>Epithelial Sodium Channels - metabolism</subject><subject>Humans</subject><subject>Hypertension - etiology</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - physiopathology</subject><subject>Ion Transport</subject><subject>Kidney - metabolism</subject><subject>Models, Biological</subject><subject>Nephrons - metabolism</subject><subject>Sodium Chloride, Dietary - administration &amp; dosage</subject><subject>Sodium Chloride, Dietary - adverse effects</subject><subject>Sodium Chloride, Dietary - metabolism</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkE9P3DAQxa2qVVn-fIUqvfUS6rG9sX2ptFotLBICxIIEJ8sk48atN1nsBMS3r2EpavEcLM-8eX76EfIV6CFABd-XtxeLy6vF2erk_Gy2nB0CywMhFHwgE5gyUYppxT-SCQUtSg1ws0N2U_pFaRYJ-ZnscC5UpZWaEL3Y-KHF4G0oVn3jx3Uxb23XYShs1xQrG4ZyhV3yg3_AYvm0wTg8P_tun3xyNiQ8eL33yPXR4mq-LE_Pj0_ms9OynnIhSmn1nap17azWKGVTsWkluFOKWuZyvtppBOGUbiRzFBoHteOQo3LZcN4A3yM_tr6b8W6NTY3dEG0wm-jXNj6Z3nrz_6TzrfnZPxippOJCZ4Nvrwaxvx8xDWbtU40h2A77MRkmFJUCKqayVG-ldexTiujevgFqntGbd-hNRm9e0OfdL__mfNv8yzoLxFbw2IcBY_odxkeMpsXMuDU0H8EqVTLKgPJc5UuL_wE2EJHh</recordid><startdate>20210303</startdate><enddate>20210303</enddate><creator>Mutchler, Stephanie M.</creator><creator>Kirabo, Annet</creator><creator>Kleyman, Thomas R.</creator><general>American Heart Association, Inc</general><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><orcidid>https://orcid.org/0000-0002-4288-4452</orcidid><orcidid>https://orcid.org/0000-0002-2413-5415</orcidid><orcidid>https://orcid.org/0000-0001-8580-9359</orcidid></search><sort><creationdate>20210303</creationdate><title>Epithelial Sodium Channel and Salt-Sensitive Hypertension</title><author>Mutchler, Stephanie M. ; Kirabo, Annet ; Kleyman, Thomas R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5344-7a9b8c9cfa99e77d625643f880a2f194cf9e14f89d72f01df1cf3100137d33d13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Blood Pressure - physiology</topic><topic>Epithelial Sodium Channels - metabolism</topic><topic>Humans</topic><topic>Hypertension - etiology</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - physiopathology</topic><topic>Ion Transport</topic><topic>Kidney - metabolism</topic><topic>Models, Biological</topic><topic>Nephrons - metabolism</topic><topic>Sodium Chloride, Dietary - administration &amp; dosage</topic><topic>Sodium Chloride, Dietary - adverse effects</topic><topic>Sodium Chloride, Dietary - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mutchler, Stephanie M.</creatorcontrib><creatorcontrib>Kirabo, Annet</creatorcontrib><creatorcontrib>Kleyman, Thomas R.</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mutchler, Stephanie M.</au><au>Kirabo, Annet</au><au>Kleyman, Thomas R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epithelial Sodium Channel and Salt-Sensitive Hypertension</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2021-03-03</date><risdate>2021</risdate><volume>77</volume><issue>3</issue><spage>759</spage><epage>767</epage><pages>759-767</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><abstract>The development of high blood pressure is influenced by genetic and environmental factors, with high salt intake being a known environmental contributor. Humans display a spectrum of sodium-sensitivity, with some individuals displaying a significant blood pressure rise in response to increased sodium intake while others experience almost no change. These differences are, in part, attributable to genetic variation in pathways involved in sodium handling and excretion. ENaC (epithelial sodium channel) is one of the key transporters responsible for the reabsorption of sodium in the distal nephron. This channel has an important role in the regulation of extracellular fluid volume and consequently blood pressure. Herein, we review the role of ENaC in the development of salt-sensitive hypertension, and present mechanistic insights into the regulation of ENaC activity and how it may accelerate sodium-induced damage and dysfunction. We discuss the traditional role of ENaC in renal sodium reabsorption and review work addressing ENaC expression and function in the brain, vasculature, and immune cells, and how this has expanded the implications for its role in the initiation and progression of salt-sensitive hypertension.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>33486988</pmid><doi>10.1161/HYPERTENSIONAHA.120.14481</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-4288-4452</orcidid><orcidid>https://orcid.org/0000-0002-2413-5415</orcidid><orcidid>https://orcid.org/0000-0001-8580-9359</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0194-911X
ispartof Hypertension (Dallas, Tex. 1979), 2021-03, Vol.77 (3), p.759-767
issn 0194-911X
1524-4563
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7878349
source MEDLINE; American Heart Association Journals; EZB-FREE-00999 freely available EZB journals
subjects Animals
Blood Pressure - physiology
Epithelial Sodium Channels - metabolism
Humans
Hypertension - etiology
Hypertension - metabolism
Hypertension - physiopathology
Ion Transport
Kidney - metabolism
Models, Biological
Nephrons - metabolism
Sodium Chloride, Dietary - administration & dosage
Sodium Chloride, Dietary - adverse effects
Sodium Chloride, Dietary - metabolism
title Epithelial Sodium Channel and Salt-Sensitive Hypertension
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T04%3A19%3A30IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Epithelial%20Sodium%20Channel%20and%20Salt-Sensitive%20Hypertension&rft.jtitle=Hypertension%20(Dallas,%20Tex.%201979)&rft.au=Mutchler,%20Stephanie%20M.&rft.date=2021-03-03&rft.volume=77&rft.issue=3&rft.spage=759&rft.epage=767&rft.pages=759-767&rft.issn=0194-911X&rft.eissn=1524-4563&rft_id=info:doi/10.1161/HYPERTENSIONAHA.120.14481&rft_dat=%3Cproquest_pubme%3E2480741628%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2480741628&rft_id=info:pmid/33486988&rfr_iscdi=true