PGE 2 EP 1 receptor inhibits vasopressin-dependent water reabsorption and sodium transport in mouse collecting duct
PGE2 regulates glomerular hemodynamics, renin secretion, and tubular transport. This study examined the contribution of PGE2 EP1 receptors to sodium and water homeostasis. Male EP1-/- mice were bred with hypertensive TTRhRen mice (Htn) to evaluate blood pressure and kidney function at 8 weeks of age...
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Veröffentlicht in: | Laboratory investigation 2018-03, Vol.98 (3), p.360 |
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creator | Nasrallah, Rania Zimpelmann, Joseph Eckert, David Ghossein, Jamie Geddes, Sean Beique, Jean-Claude Thibodeau, Jean-Francois Kennedy, Chris R J Burns, Kevin D Hébert, Richard L |
description | PGE2 regulates glomerular hemodynamics, renin secretion, and tubular transport. This study examined the contribution of PGE2 EP1 receptors to sodium and water homeostasis. Male EP1-/- mice were bred with hypertensive TTRhRen mice (Htn) to evaluate blood pressure and kidney function at 8 weeks of age in four groups: wildtype (WT), EP1-/-, Htn, HtnEP1-/-. Blood pressure and water balance were unaffected by EP1 deletion. COX1 and mPGE2 synthase were increased and COX2 was decreased in mice lacking EP1, with increases in EP3 and reductions in EP2 and EP4 mRNA throughout the nephron. Microdissected proximal tubule sglt1, NHE3, and AQP1 were increased in HtnEP1-/-, but sglt2 was increased in EP1-/- mice. Thick ascending limb NKCC2 was reduced in the cortex but increased in the medulla. Inner medullary collecting duct (IMCD) AQP1 and ENaC were increased, but AVP V2 receptors and urea transporter-1 were reduced in all mice compared to WT. In WT and Htn mice, PGE2 inhibited AVP-water transport and increased calcium in the IMCD, and inhibited sodium transport in cortical collecting ducts, but not in EP1-/- or HtnEP1-/- mice. Amiloride (ENaC) and hydrochlorothiazide (pendrin inhibitor) equally attenuated the effect of PGE2 on sodium transport. Taken together, the data suggest that EP1 regulates renal aquaporins and sodium transporters, attenuates AVP-water transport and inhibits sodium transport in the mouse collecting duct, which is mediated by both ENaC and pendrin-dependent pathways. |
doi_str_mv | 10.1038/labinvest.2017.133 |
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This study examined the contribution of PGE2 EP1 receptors to sodium and water homeostasis. Male EP1-/- mice were bred with hypertensive TTRhRen mice (Htn) to evaluate blood pressure and kidney function at 8 weeks of age in four groups: wildtype (WT), EP1-/-, Htn, HtnEP1-/-. Blood pressure and water balance were unaffected by EP1 deletion. COX1 and mPGE2 synthase were increased and COX2 was decreased in mice lacking EP1, with increases in EP3 and reductions in EP2 and EP4 mRNA throughout the nephron. Microdissected proximal tubule sglt1, NHE3, and AQP1 were increased in HtnEP1-/-, but sglt2 was increased in EP1-/- mice. Thick ascending limb NKCC2 was reduced in the cortex but increased in the medulla. Inner medullary collecting duct (IMCD) AQP1 and ENaC were increased, but AVP V2 receptors and urea transporter-1 were reduced in all mice compared to WT. In WT and Htn mice, PGE2 inhibited AVP-water transport and increased calcium in the IMCD, and inhibited sodium transport in cortical collecting ducts, but not in EP1-/- or HtnEP1-/- mice. Amiloride (ENaC) and hydrochlorothiazide (pendrin inhibitor) equally attenuated the effect of PGE2 on sodium transport. Taken together, the data suggest that EP1 regulates renal aquaporins and sodium transporters, attenuates AVP-water transport and inhibits sodium transport in the mouse collecting duct, which is mediated by both ENaC and pendrin-dependent pathways.</description><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/labinvest.2017.133</identifier><identifier>PMID: 29251736</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Aquaporins - metabolism ; Blood Pressure ; Calcium - metabolism ; Dinoprostone - metabolism ; Glomerular Filtration Rate ; Hypertension - metabolism ; Kidney Tubules, Collecting - metabolism ; Male ; Mice ; Prostaglandin-E Synthases - metabolism ; Prostaglandin-Endoperoxide Synthases - metabolism ; Receptors, Prostaglandin E, EP1 Subtype - metabolism ; Sodium - metabolism ; Sodium-Hydrogen Exchanger 3 - metabolism ; Solute Carrier Family 12, Member 1 - metabolism</subject><ispartof>Laboratory investigation, 2018-03, Vol.98 (3), p.360</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></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/29251736$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nasrallah, Rania</creatorcontrib><creatorcontrib>Zimpelmann, Joseph</creatorcontrib><creatorcontrib>Eckert, David</creatorcontrib><creatorcontrib>Ghossein, Jamie</creatorcontrib><creatorcontrib>Geddes, Sean</creatorcontrib><creatorcontrib>Beique, Jean-Claude</creatorcontrib><creatorcontrib>Thibodeau, Jean-Francois</creatorcontrib><creatorcontrib>Kennedy, Chris R J</creatorcontrib><creatorcontrib>Burns, Kevin D</creatorcontrib><creatorcontrib>Hébert, Richard L</creatorcontrib><title>PGE 2 EP 1 receptor inhibits vasopressin-dependent water reabsorption and sodium transport in mouse collecting duct</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><description>PGE2 regulates glomerular hemodynamics, renin secretion, and tubular transport. This study examined the contribution of PGE2 EP1 receptors to sodium and water homeostasis. Male EP1-/- mice were bred with hypertensive TTRhRen mice (Htn) to evaluate blood pressure and kidney function at 8 weeks of age in four groups: wildtype (WT), EP1-/-, Htn, HtnEP1-/-. Blood pressure and water balance were unaffected by EP1 deletion. COX1 and mPGE2 synthase were increased and COX2 was decreased in mice lacking EP1, with increases in EP3 and reductions in EP2 and EP4 mRNA throughout the nephron. Microdissected proximal tubule sglt1, NHE3, and AQP1 were increased in HtnEP1-/-, but sglt2 was increased in EP1-/- mice. Thick ascending limb NKCC2 was reduced in the cortex but increased in the medulla. Inner medullary collecting duct (IMCD) AQP1 and ENaC were increased, but AVP V2 receptors and urea transporter-1 were reduced in all mice compared to WT. In WT and Htn mice, PGE2 inhibited AVP-water transport and increased calcium in the IMCD, and inhibited sodium transport in cortical collecting ducts, but not in EP1-/- or HtnEP1-/- mice. Amiloride (ENaC) and hydrochlorothiazide (pendrin inhibitor) equally attenuated the effect of PGE2 on sodium transport. Taken together, the data suggest that EP1 regulates renal aquaporins and sodium transporters, attenuates AVP-water transport and inhibits sodium transport in the mouse collecting duct, which is mediated by both ENaC and pendrin-dependent pathways.</description><subject>Animals</subject><subject>Aquaporins - metabolism</subject><subject>Blood Pressure</subject><subject>Calcium - metabolism</subject><subject>Dinoprostone - metabolism</subject><subject>Glomerular Filtration Rate</subject><subject>Hypertension - metabolism</subject><subject>Kidney Tubules, Collecting - metabolism</subject><subject>Male</subject><subject>Mice</subject><subject>Prostaglandin-E Synthases - metabolism</subject><subject>Prostaglandin-Endoperoxide Synthases - metabolism</subject><subject>Receptors, Prostaglandin E, EP1 Subtype - metabolism</subject><subject>Sodium - metabolism</subject><subject>Sodium-Hydrogen Exchanger 3 - metabolism</subject><subject>Solute Carrier Family 12, Member 1 - metabolism</subject><issn>1530-0307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo1j99KwzAchYMgbk5fwAvJC3Tmb9NeypibMHAXux9J86tG2iQk6cS3t6BeHT44fJyD0AMla0p48zRo4_wFclkzQtWacn6FllRyUhFO1ALd5vxJCBWiljdowVomqeL1EuXjbosZ3h4xxQk6iCUk7PyHM65kfNE5xAQ5O19ZiOAt-IK_dIE0t7XJIcXigsfaW5yDddOIS9I-x5DKrMFjmDLgLgwDdMX5d2ynrtyh614PGe7_coVOL9vTZl8d3navm-dDFVteqt5Co0CCZH1retrDPFo0zArO5MycqVZToEJy02qidFdDLZqWEAXCyJ7wFXr81cbJjGDPMblRp-_z_3n-A3r9Xfg</recordid><startdate>201803</startdate><enddate>201803</enddate><creator>Nasrallah, Rania</creator><creator>Zimpelmann, Joseph</creator><creator>Eckert, David</creator><creator>Ghossein, Jamie</creator><creator>Geddes, Sean</creator><creator>Beique, Jean-Claude</creator><creator>Thibodeau, Jean-Francois</creator><creator>Kennedy, Chris R J</creator><creator>Burns, Kevin D</creator><creator>Hébert, Richard L</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>201803</creationdate><title>PGE 2 EP 1 receptor inhibits vasopressin-dependent water reabsorption and sodium transport in mouse collecting duct</title><author>Nasrallah, Rania ; Zimpelmann, Joseph ; Eckert, David ; Ghossein, Jamie ; Geddes, Sean ; Beique, Jean-Claude ; Thibodeau, Jean-Francois ; Kennedy, Chris R J ; Burns, Kevin D ; Hébert, Richard L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p93t-fde87e5e52f9bf1fe292482d4325bf13279a1e1453b9a07ac6e6489007e4b5f03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Aquaporins - metabolism</topic><topic>Blood Pressure</topic><topic>Calcium - metabolism</topic><topic>Dinoprostone - metabolism</topic><topic>Glomerular Filtration Rate</topic><topic>Hypertension - metabolism</topic><topic>Kidney Tubules, Collecting - metabolism</topic><topic>Male</topic><topic>Mice</topic><topic>Prostaglandin-E Synthases - metabolism</topic><topic>Prostaglandin-Endoperoxide Synthases - metabolism</topic><topic>Receptors, Prostaglandin E, EP1 Subtype - metabolism</topic><topic>Sodium - metabolism</topic><topic>Sodium-Hydrogen Exchanger 3 - metabolism</topic><topic>Solute Carrier Family 12, Member 1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nasrallah, Rania</creatorcontrib><creatorcontrib>Zimpelmann, Joseph</creatorcontrib><creatorcontrib>Eckert, David</creatorcontrib><creatorcontrib>Ghossein, Jamie</creatorcontrib><creatorcontrib>Geddes, Sean</creatorcontrib><creatorcontrib>Beique, Jean-Claude</creatorcontrib><creatorcontrib>Thibodeau, Jean-Francois</creatorcontrib><creatorcontrib>Kennedy, Chris R J</creatorcontrib><creatorcontrib>Burns, Kevin D</creatorcontrib><creatorcontrib>Hébert, Richard L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Laboratory investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nasrallah, Rania</au><au>Zimpelmann, Joseph</au><au>Eckert, David</au><au>Ghossein, Jamie</au><au>Geddes, Sean</au><au>Beique, Jean-Claude</au><au>Thibodeau, Jean-Francois</au><au>Kennedy, Chris R J</au><au>Burns, Kevin D</au><au>Hébert, Richard L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PGE 2 EP 1 receptor inhibits vasopressin-dependent water reabsorption and sodium transport in mouse collecting duct</atitle><jtitle>Laboratory investigation</jtitle><addtitle>Lab Invest</addtitle><date>2018-03</date><risdate>2018</risdate><volume>98</volume><issue>3</issue><spage>360</spage><pages>360-</pages><eissn>1530-0307</eissn><abstract>PGE2 regulates glomerular hemodynamics, renin secretion, and tubular transport. This study examined the contribution of PGE2 EP1 receptors to sodium and water homeostasis. Male EP1-/- mice were bred with hypertensive TTRhRen mice (Htn) to evaluate blood pressure and kidney function at 8 weeks of age in four groups: wildtype (WT), EP1-/-, Htn, HtnEP1-/-. Blood pressure and water balance were unaffected by EP1 deletion. COX1 and mPGE2 synthase were increased and COX2 was decreased in mice lacking EP1, with increases in EP3 and reductions in EP2 and EP4 mRNA throughout the nephron. Microdissected proximal tubule sglt1, NHE3, and AQP1 were increased in HtnEP1-/-, but sglt2 was increased in EP1-/- mice. Thick ascending limb NKCC2 was reduced in the cortex but increased in the medulla. Inner medullary collecting duct (IMCD) AQP1 and ENaC were increased, but AVP V2 receptors and urea transporter-1 were reduced in all mice compared to WT. In WT and Htn mice, PGE2 inhibited AVP-water transport and increased calcium in the IMCD, and inhibited sodium transport in cortical collecting ducts, but not in EP1-/- or HtnEP1-/- mice. Amiloride (ENaC) and hydrochlorothiazide (pendrin inhibitor) equally attenuated the effect of PGE2 on sodium transport. Taken together, the data suggest that EP1 regulates renal aquaporins and sodium transporters, attenuates AVP-water transport and inhibits sodium transport in the mouse collecting duct, which is mediated by both ENaC and pendrin-dependent pathways.</abstract><cop>United States</cop><pmid>29251736</pmid><doi>10.1038/labinvest.2017.133</doi></addata></record> |
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subjects | Animals Aquaporins - metabolism Blood Pressure Calcium - metabolism Dinoprostone - metabolism Glomerular Filtration Rate Hypertension - metabolism Kidney Tubules, Collecting - metabolism Male Mice Prostaglandin-E Synthases - metabolism Prostaglandin-Endoperoxide Synthases - metabolism Receptors, Prostaglandin E, EP1 Subtype - metabolism Sodium - metabolism Sodium-Hydrogen Exchanger 3 - metabolism Solute Carrier Family 12, Member 1 - metabolism |
title | PGE 2 EP 1 receptor inhibits vasopressin-dependent water reabsorption and sodium transport in mouse collecting duct |
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