Na+/H+ exchange activity and NHE-3 expression in renal tubules from the spontaneously hypertensive rat
Na+/H+ exchange activity and NHE-3 expression in renal tubules from the spontaneously hypertensive rat. The NHE-3 isoform of the Na+/H+ antiporter, in the apical membrane of renal proximal tubule, is responsible for the bulk transport of Na+ and fluid reabsorption. Studies have reported that apical...
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| description | Na+/H+ exchange activity and NHE-3 expression in renal tubules from the spontaneously hypertensive rat.
The NHE-3 isoform of the Na+/H+ antiporter, in the apical membrane of renal proximal tubule, is responsible for the bulk transport of Na+ and fluid reabsorption. Studies have reported that apical NHE-3 translocates to internal pools, thereby facilitating natriuresis when blood pressure increases abruptly.
The present study examined Na+/H+ exchange activity and NHE-3 expression in renal cortical tubules from the spontaneously hypertensive rat (SHR) and WKY rats before and after the development of hypertension. SHR 4 to 6 weeks of age were pre-hypertensive, 6 to 7 weeks old had mild hypertension, and 8 to 13 weeks old had severe hypertension. Renal proximal tubules (PTs) were isolated and purified by Percoll gradient centrifugation. NHE-3 protein and mRNA levels were determined by Western and Northern blots, respectively. Apical brush border membrane vesicles (BBMV) were prepared using the MgSO4 aggregation method and Na+/H+ exchange activity assessed using the acridine orange method.
Na+/H+ exchange activity, determined as the rate of Na+-dependent intracellular pH (pHi) recovery assessed using BCECF after an acute acid load, was significantly greater in PTs from SHR than in WKY rats at all age groups (4 to 6 weeks, 0.30 ± 0.04 vs. 0.24 ± 0.02 pH U/30 sec, P < 0.05; 6 to 7 weeks, 0.42 ± 0.07 vs. 0.29 ± 0.05 pH U/30 sec, P < 0.05; and 8 to 13 weeks, 0.48 ± 0.07 vs. 0.40 ± 0.07 pH U/30 sec, P < 0.05). The Na+-dependent recovery in BBMV was also greater in SHR than WKY rats (1464 ± 62 vs. 1042 ± 79 fluorescence. U/5 sec, P < 0.001) and was unaffected by cariporide, a specific NHE-1 inhibitor. NHE-3 protein levels also were significantly higher in SHR than age-matched WKY rats at all stages during the development of hypertension (pre-hypertensive 1.8-fold; early onset hypertension twofold; established hypertension 1.5-fold; each P < 0.05). By contrast, NHE-3 mRNA levels were not different between SHR and WKY rats at each age group.
Na+/H+ exchange activity and NHE-3 protein abundance in renal proximal tubules from the SHR are increased while NHE-3 mRNA is not. A post-transcriptional event(s) best explains the increase in NHE-3 protein expression since mRNA levels were not increased. The alterations in the SHR antedate the development of hypertension and fail to decrease as blood pressure increases with age in the SHR, which likely results in inappropriate ren |
| doi_str_mv | 10.1046/j.1523-1755.2002.00406.x |
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The NHE-3 isoform of the Na+/H+ antiporter, in the apical membrane of renal proximal tubule, is responsible for the bulk transport of Na+ and fluid reabsorption. Studies have reported that apical NHE-3 translocates to internal pools, thereby facilitating natriuresis when blood pressure increases abruptly.
The present study examined Na+/H+ exchange activity and NHE-3 expression in renal cortical tubules from the spontaneously hypertensive rat (SHR) and WKY rats before and after the development of hypertension. SHR 4 to 6 weeks of age were pre-hypertensive, 6 to 7 weeks old had mild hypertension, and 8 to 13 weeks old had severe hypertension. Renal proximal tubules (PTs) were isolated and purified by Percoll gradient centrifugation. NHE-3 protein and mRNA levels were determined by Western and Northern blots, respectively. Apical brush border membrane vesicles (BBMV) were prepared using the MgSO4 aggregation method and Na+/H+ exchange activity assessed using the acridine orange method.
Na+/H+ exchange activity, determined as the rate of Na+-dependent intracellular pH (pHi) recovery assessed using BCECF after an acute acid load, was significantly greater in PTs from SHR than in WKY rats at all age groups (4 to 6 weeks, 0.30 ± 0.04 vs. 0.24 ± 0.02 pH U/30 sec, P < 0.05; 6 to 7 weeks, 0.42 ± 0.07 vs. 0.29 ± 0.05 pH U/30 sec, P < 0.05; and 8 to 13 weeks, 0.48 ± 0.07 vs. 0.40 ± 0.07 pH U/30 sec, P < 0.05). The Na+-dependent recovery in BBMV was also greater in SHR than WKY rats (1464 ± 62 vs. 1042 ± 79 fluorescence. U/5 sec, P < 0.001) and was unaffected by cariporide, a specific NHE-1 inhibitor. NHE-3 protein levels also were significantly higher in SHR than age-matched WKY rats at all stages during the development of hypertension (pre-hypertensive 1.8-fold; early onset hypertension twofold; established hypertension 1.5-fold; each P < 0.05). By contrast, NHE-3 mRNA levels were not different between SHR and WKY rats at each age group.
Na+/H+ exchange activity and NHE-3 protein abundance in renal proximal tubules from the SHR are increased while NHE-3 mRNA is not. A post-transcriptional event(s) best explains the increase in NHE-3 protein expression since mRNA levels were not increased. The alterations in the SHR antedate the development of hypertension and fail to decrease as blood pressure increases with age in the SHR, which likely results in inappropriate renal sodium retention in the face of a chronic rise in blood pressure.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1046/j.1523-1755.2002.00406.x</identifier><identifier>PMID: 12081574</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; blood pressure ; Cardiology. Vascular system ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; genetics ; Hypertension - metabolism ; inbred SHR ; ion transport ; kidney ; Kidney Tubules, Proximal - metabolism ; Kidney Tubules, Proximal - ultrastructure ; Medical sciences ; membranes ; Microvilli - metabolism ; natriuresis ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; RNA, Messenger - analysis ; Sodium - metabolism ; sodium-hydrogen antiporter ; Sodium-Hydrogen Exchanger 3 ; Sodium-Hydrogen Exchangers - analysis ; Sodium-Hydrogen Exchangers - genetics</subject><ispartof>Kidney international, 2002-07, Vol.62 (1), p.157-165</ispartof><rights>2002 International Society of Nephrology</rights><rights>2002 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jul 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c480x-1691e74e170a8261df0037d7927eb0671d064a3d5c02fd05b016f3ed57008b113</citedby><cites>FETCH-LOGICAL-c480x-1691e74e170a8261df0037d7927eb0671d064a3d5c02fd05b016f3ed57008b113</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/210121346?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13738605$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12081574$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lapointe, Michael S.</creatorcontrib><creatorcontrib>Sodhi, Chhinder</creatorcontrib><creatorcontrib>Sahai, Atul</creatorcontrib><creatorcontrib>Batlle, Daniel</creatorcontrib><title>Na+/H+ exchange activity and NHE-3 expression in renal tubules from the spontaneously hypertensive rat</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Na+/H+ exchange activity and NHE-3 expression in renal tubules from the spontaneously hypertensive rat.
The NHE-3 isoform of the Na+/H+ antiporter, in the apical membrane of renal proximal tubule, is responsible for the bulk transport of Na+ and fluid reabsorption. Studies have reported that apical NHE-3 translocates to internal pools, thereby facilitating natriuresis when blood pressure increases abruptly.
The present study examined Na+/H+ exchange activity and NHE-3 expression in renal cortical tubules from the spontaneously hypertensive rat (SHR) and WKY rats before and after the development of hypertension. SHR 4 to 6 weeks of age were pre-hypertensive, 6 to 7 weeks old had mild hypertension, and 8 to 13 weeks old had severe hypertension. Renal proximal tubules (PTs) were isolated and purified by Percoll gradient centrifugation. NHE-3 protein and mRNA levels were determined by Western and Northern blots, respectively. Apical brush border membrane vesicles (BBMV) were prepared using the MgSO4 aggregation method and Na+/H+ exchange activity assessed using the acridine orange method.
Na+/H+ exchange activity, determined as the rate of Na+-dependent intracellular pH (pHi) recovery assessed using BCECF after an acute acid load, was significantly greater in PTs from SHR than in WKY rats at all age groups (4 to 6 weeks, 0.30 ± 0.04 vs. 0.24 ± 0.02 pH U/30 sec, P < 0.05; 6 to 7 weeks, 0.42 ± 0.07 vs. 0.29 ± 0.05 pH U/30 sec, P < 0.05; and 8 to 13 weeks, 0.48 ± 0.07 vs. 0.40 ± 0.07 pH U/30 sec, P < 0.05). The Na+-dependent recovery in BBMV was also greater in SHR than WKY rats (1464 ± 62 vs. 1042 ± 79 fluorescence. U/5 sec, P < 0.001) and was unaffected by cariporide, a specific NHE-1 inhibitor. NHE-3 protein levels also were significantly higher in SHR than age-matched WKY rats at all stages during the development of hypertension (pre-hypertensive 1.8-fold; early onset hypertension twofold; established hypertension 1.5-fold; each P < 0.05). By contrast, NHE-3 mRNA levels were not different between SHR and WKY rats at each age group.
Na+/H+ exchange activity and NHE-3 protein abundance in renal proximal tubules from the SHR are increased while NHE-3 mRNA is not. A post-transcriptional event(s) best explains the increase in NHE-3 protein expression since mRNA levels were not increased. The alterations in the SHR antedate the development of hypertension and fail to decrease as blood pressure increases with age in the SHR, which likely results in inappropriate renal sodium retention in the face of a chronic rise in blood pressure.</description><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>blood pressure</subject><subject>Cardiology. Vascular system</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>genetics</subject><subject>Hypertension - metabolism</subject><subject>inbred SHR</subject><subject>ion transport</subject><subject>kidney</subject><subject>Kidney Tubules, Proximal - metabolism</subject><subject>Kidney Tubules, Proximal - ultrastructure</subject><subject>Medical sciences</subject><subject>membranes</subject><subject>Microvilli - metabolism</subject><subject>natriuresis</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>RNA, Messenger - analysis</subject><subject>Sodium - metabolism</subject><subject>sodium-hydrogen antiporter</subject><subject>Sodium-Hydrogen Exchanger 3</subject><subject>Sodium-Hydrogen Exchangers - analysis</subject><subject>Sodium-Hydrogen Exchangers - genetics</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqFkU9v1DAQxSMEokvhI4AsJLhUScf_4uwRqraLVJULnC3HmbBeZZ1gJ6vdb49DVq3EhdNo9H4zmnkvywiFgoIor3cFlYznVElZMABWAAgoi-OLbPUkvMxWAJXMmeTVRfYmxh2kfs3hdXZBGVRUKrHK2kdzdb25Ini0W-N_ITF2dAc3nojxDXnc3OY8aUPAGF3vifMkoDcdGad66jCSNvR7Mm6RxKH3o_HYT7E7ke1pwDCij-6AJJjxbfaqNV3Ed-d6mf28u_1xs8kfvt9_u_nykFtRwTGn5ZqiEkgVmIqVtGkBuGrUmimsoVS0gVIY3kgLrG1A1kDLlmMjVXqtppRfZp-XvUPof08YR7130WLXLZdpRSspmBAJ_PgPuOunkD6LmlGgjHJRJqhaIBv6GAO2eghub8JJU9BzEHqnZ7_17Leeg9B_g9DHNPrhvH-q99g8D56dT8CnM2CiNV0bjLcuPnNc8aoEmbj3C-fNOAV8AoRIUVaz_nXRMdl6cBh0tA69xcYFtKNuevf_a_8A91qu0g</recordid><startdate>200207</startdate><enddate>200207</enddate><creator>Lapointe, Michael S.</creator><creator>Sodhi, Chhinder</creator><creator>Sahai, Atul</creator><creator>Batlle, Daniel</creator><general>Elsevier Inc</general><general>Nature Publishing</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>200207</creationdate><title>Na+/H+ exchange activity and NHE-3 expression in renal tubules from the spontaneously hypertensive rat</title><author>Lapointe, Michael S. ; Sodhi, Chhinder ; Sahai, Atul ; Batlle, Daniel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c480x-1691e74e170a8261df0037d7927eb0671d064a3d5c02fd05b016f3ed57008b113</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>blood pressure</topic><topic>Cardiology. Vascular system</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>genetics</topic><topic>Hypertension - metabolism</topic><topic>inbred SHR</topic><topic>ion transport</topic><topic>kidney</topic><topic>Kidney Tubules, Proximal - metabolism</topic><topic>Kidney Tubules, Proximal - ultrastructure</topic><topic>Medical sciences</topic><topic>membranes</topic><topic>Microvilli - metabolism</topic><topic>natriuresis</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>RNA, Messenger - analysis</topic><topic>Sodium - metabolism</topic><topic>sodium-hydrogen antiporter</topic><topic>Sodium-Hydrogen Exchanger 3</topic><topic>Sodium-Hydrogen Exchangers - analysis</topic><topic>Sodium-Hydrogen Exchangers - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lapointe, Michael S.</creatorcontrib><creatorcontrib>Sodhi, Chhinder</creatorcontrib><creatorcontrib>Sahai, Atul</creatorcontrib><creatorcontrib>Batlle, Daniel</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lapointe, Michael S.</au><au>Sodhi, Chhinder</au><au>Sahai, Atul</au><au>Batlle, Daniel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Na+/H+ exchange activity and NHE-3 expression in renal tubules from the spontaneously hypertensive rat</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2002-07</date><risdate>2002</risdate><volume>62</volume><issue>1</issue><spage>157</spage><epage>165</epage><pages>157-165</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Na+/H+ exchange activity and NHE-3 expression in renal tubules from the spontaneously hypertensive rat.
The NHE-3 isoform of the Na+/H+ antiporter, in the apical membrane of renal proximal tubule, is responsible for the bulk transport of Na+ and fluid reabsorption. Studies have reported that apical NHE-3 translocates to internal pools, thereby facilitating natriuresis when blood pressure increases abruptly.
The present study examined Na+/H+ exchange activity and NHE-3 expression in renal cortical tubules from the spontaneously hypertensive rat (SHR) and WKY rats before and after the development of hypertension. SHR 4 to 6 weeks of age were pre-hypertensive, 6 to 7 weeks old had mild hypertension, and 8 to 13 weeks old had severe hypertension. Renal proximal tubules (PTs) were isolated and purified by Percoll gradient centrifugation. NHE-3 protein and mRNA levels were determined by Western and Northern blots, respectively. Apical brush border membrane vesicles (BBMV) were prepared using the MgSO4 aggregation method and Na+/H+ exchange activity assessed using the acridine orange method.
Na+/H+ exchange activity, determined as the rate of Na+-dependent intracellular pH (pHi) recovery assessed using BCECF after an acute acid load, was significantly greater in PTs from SHR than in WKY rats at all age groups (4 to 6 weeks, 0.30 ± 0.04 vs. 0.24 ± 0.02 pH U/30 sec, P < 0.05; 6 to 7 weeks, 0.42 ± 0.07 vs. 0.29 ± 0.05 pH U/30 sec, P < 0.05; and 8 to 13 weeks, 0.48 ± 0.07 vs. 0.40 ± 0.07 pH U/30 sec, P < 0.05). The Na+-dependent recovery in BBMV was also greater in SHR than WKY rats (1464 ± 62 vs. 1042 ± 79 fluorescence. U/5 sec, P < 0.001) and was unaffected by cariporide, a specific NHE-1 inhibitor. NHE-3 protein levels also were significantly higher in SHR than age-matched WKY rats at all stages during the development of hypertension (pre-hypertensive 1.8-fold; early onset hypertension twofold; established hypertension 1.5-fold; each P < 0.05). By contrast, NHE-3 mRNA levels were not different between SHR and WKY rats at each age group.
Na+/H+ exchange activity and NHE-3 protein abundance in renal proximal tubules from the SHR are increased while NHE-3 mRNA is not. A post-transcriptional event(s) best explains the increase in NHE-3 protein expression since mRNA levels were not increased. The alterations in the SHR antedate the development of hypertension and fail to decrease as blood pressure increases with age in the SHR, which likely results in inappropriate renal sodium retention in the face of a chronic rise in blood pressure.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>12081574</pmid><doi>10.1046/j.1523-1755.2002.00406.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels blood pressure Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology genetics Hypertension - metabolism inbred SHR ion transport kidney Kidney Tubules, Proximal - metabolism Kidney Tubules, Proximal - ultrastructure Medical sciences membranes Microvilli - metabolism natriuresis Rats Rats, Inbred SHR Rats, Inbred WKY RNA, Messenger - analysis Sodium - metabolism sodium-hydrogen antiporter Sodium-Hydrogen Exchanger 3 Sodium-Hydrogen Exchangers - analysis Sodium-Hydrogen Exchangers - genetics |
| title | Na+/H+ exchange activity and NHE-3 expression in renal tubules from the spontaneously hypertensive rat |
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