Thromboxane prostanoid receptors enhance contractions, endothelin-1, and oxidative stress in microvessels from mice with chronic kidney disease
Cardiovascular disease is frequent in chronic kidney disease and has been related to angiotensin II, endothelin-1 (ET-1), thromboxane A2, and reactive oxygen species (ROS). Because activation of thromboxane prostanoid receptors (TP-Rs) can generate ROS, which can generate ET-1, we tested the hypothe...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2015-05, Vol.65 (5), p.1055-1063 |
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| creator | Wang, Cheng Luo, Zaiming Kohan, Donald Wellstein, Anton Jose, Pedro A Welch, William J Wilcox, Christopher S Wang, Dan |
| description | Cardiovascular disease is frequent in chronic kidney disease and has been related to angiotensin II, endothelin-1 (ET-1), thromboxane A2, and reactive oxygen species (ROS). Because activation of thromboxane prostanoid receptors (TP-Rs) can generate ROS, which can generate ET-1, we tested the hypothesis that chronic kidney disease induces cyclooxygenase-2 whose products activate TP-Rs to enhance ET-1 and ROS generation and contractions. Mesenteric resistance arterioles were isolated from C57/BL6 or TP-R+/+ and TP-R-/- mice 3 months after SHAM-operation (SHAM) or surgical reduced renal mass (RRM, n=6/group). Microvascular contractions were studied on a wire myograph. Cellular (ethidium: dihydroethidium) and mitochondrial (mitoSOX) ROS were measured by fluorescence microscopy. Mice with RRM had increased excretion of markers of oxidative stress, thromboxane, and microalbumin; increased plasma ET-1; and increased microvascular expression of p22(phox), cyclooxygenase-2, TP-Rs, preproendothelin and endothelin-A receptors, and increased arteriolar remodeling. They had increased contractions to U-46,619 (118 ± 3 versus 87 ± 6, P |
| doi_str_mv | 10.1161/HYPERTENSIONAHA.115.05244 |
| format | Article |
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Because activation of thromboxane prostanoid receptors (TP-Rs) can generate ROS, which can generate ET-1, we tested the hypothesis that chronic kidney disease induces cyclooxygenase-2 whose products activate TP-Rs to enhance ET-1 and ROS generation and contractions. Mesenteric resistance arterioles were isolated from C57/BL6 or TP-R+/+ and TP-R-/- mice 3 months after SHAM-operation (SHAM) or surgical reduced renal mass (RRM, n=6/group). Microvascular contractions were studied on a wire myograph. Cellular (ethidium: dihydroethidium) and mitochondrial (mitoSOX) ROS were measured by fluorescence microscopy. Mice with RRM had increased excretion of markers of oxidative stress, thromboxane, and microalbumin; increased plasma ET-1; and increased microvascular expression of p22(phox), cyclooxygenase-2, TP-Rs, preproendothelin and endothelin-A receptors, and increased arteriolar remodeling. They had increased contractions to U-46,619 (118 ± 3 versus 87 ± 6, P<0.05) and ET-1 (108 ± 5 versus 89 ± 4, P<0.05), which were dependent on cellular and mitochondrial ROS, cyclooxygenase-2, and TP-Rs. RRM doubled the ET-1-induced cellular and mitochondrial ROS generation (P<0.05). TP-R-/- mice with RRM lacked these abnormal structural and functional microvascular responses and lacked the increased systemic and the increased microvascular oxidative stress and circulating ET-1. In conclusion, RRM leads to microvascular remodeling and enhanced ET-1-induced cellular and mitochondrial ROS and contractions that are mediated by cyclooxygenase-2 products activating TP-Rs. Thus, TP-Rs can be upstream from enhanced ROS, ET-1, microvascular remodeling, and contractility and may thereby coordinate vascular dysfunction in chronic kidney disease.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/HYPERTENSIONAHA.115.05244</identifier><identifier>PMID: 25733239</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Arterioles - metabolism ; Arterioles - physiopathology ; Disease Models, Animal ; Endothelin-1 - biosynthesis ; Endothelin-1 - genetics ; Gene Expression Regulation ; Kidney - blood supply ; Male ; Mice ; Mice, Inbred C57BL ; Oxidative Stress ; Reactive Oxygen Species - metabolism ; Real-Time Polymerase Chain Reaction ; Receptors, Thromboxane - biosynthesis ; Receptors, Thromboxane - genetics ; Renal Circulation ; Renal Insufficiency, Chronic - genetics ; Renal Insufficiency, Chronic - metabolism ; Renal Insufficiency, Chronic - physiopathology ; RNA - genetics ; Vascular Remodeling ; Vasoconstriction</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2015-05, Vol.65 (5), p.1055-1063</ispartof><rights>2015 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c368t-34b56de9a0fba48d9ce66c9f75dc180ff2e05a9bb3405ffee06fd51729af2ed83</citedby><cites>FETCH-LOGICAL-c368t-34b56de9a0fba48d9ce66c9f75dc180ff2e05a9bb3405ffee06fd51729af2ed83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3678,27915,27916</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25733239$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Cheng</creatorcontrib><creatorcontrib>Luo, Zaiming</creatorcontrib><creatorcontrib>Kohan, Donald</creatorcontrib><creatorcontrib>Wellstein, Anton</creatorcontrib><creatorcontrib>Jose, Pedro A</creatorcontrib><creatorcontrib>Welch, William J</creatorcontrib><creatorcontrib>Wilcox, Christopher S</creatorcontrib><creatorcontrib>Wang, Dan</creatorcontrib><title>Thromboxane prostanoid receptors enhance contractions, endothelin-1, and oxidative stress in microvessels from mice with chronic kidney disease</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>Cardiovascular disease is frequent in chronic kidney disease and has been related to angiotensin II, endothelin-1 (ET-1), thromboxane A2, and reactive oxygen species (ROS). Because activation of thromboxane prostanoid receptors (TP-Rs) can generate ROS, which can generate ET-1, we tested the hypothesis that chronic kidney disease induces cyclooxygenase-2 whose products activate TP-Rs to enhance ET-1 and ROS generation and contractions. Mesenteric resistance arterioles were isolated from C57/BL6 or TP-R+/+ and TP-R-/- mice 3 months after SHAM-operation (SHAM) or surgical reduced renal mass (RRM, n=6/group). Microvascular contractions were studied on a wire myograph. Cellular (ethidium: dihydroethidium) and mitochondrial (mitoSOX) ROS were measured by fluorescence microscopy. Mice with RRM had increased excretion of markers of oxidative stress, thromboxane, and microalbumin; increased plasma ET-1; and increased microvascular expression of p22(phox), cyclooxygenase-2, TP-Rs, preproendothelin and endothelin-A receptors, and increased arteriolar remodeling. They had increased contractions to U-46,619 (118 ± 3 versus 87 ± 6, P<0.05) and ET-1 (108 ± 5 versus 89 ± 4, P<0.05), which were dependent on cellular and mitochondrial ROS, cyclooxygenase-2, and TP-Rs. RRM doubled the ET-1-induced cellular and mitochondrial ROS generation (P<0.05). TP-R-/- mice with RRM lacked these abnormal structural and functional microvascular responses and lacked the increased systemic and the increased microvascular oxidative stress and circulating ET-1. In conclusion, RRM leads to microvascular remodeling and enhanced ET-1-induced cellular and mitochondrial ROS and contractions that are mediated by cyclooxygenase-2 products activating TP-Rs. Thus, TP-Rs can be upstream from enhanced ROS, ET-1, microvascular remodeling, and contractility and may thereby coordinate vascular dysfunction in chronic kidney disease.</description><subject>Animals</subject><subject>Arterioles - metabolism</subject><subject>Arterioles - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Endothelin-1 - biosynthesis</subject><subject>Endothelin-1 - genetics</subject><subject>Gene Expression Regulation</subject><subject>Kidney - blood supply</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Oxidative Stress</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Receptors, Thromboxane - biosynthesis</subject><subject>Receptors, Thromboxane - genetics</subject><subject>Renal Circulation</subject><subject>Renal Insufficiency, Chronic - genetics</subject><subject>Renal Insufficiency, Chronic - metabolism</subject><subject>Renal Insufficiency, Chronic - physiopathology</subject><subject>RNA - genetics</subject><subject>Vascular Remodeling</subject><subject>Vasoconstriction</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdUctuFDEQtBCIbAK_gMyNQyaxx49ZH1fRho0UJQgWCU4jj93WGmbsxfaG5Cvyy_HmwYFTq6uru1RdCH2k5IRSSU9XP78sv66XV98urq8Wq0UFxQkRLeev0IzW2nAh2Ws0I1TxRlH64wAd5vyLEMo5796ig1Z0jLVMzdD9epPiNMRbHQBvU8xFh-gtTmBgW2LKGMJGBwPYxFCSNsXHkI8ramPZwOhDQ4-xDhbHW2918TeAc0mQM_YBT96keFMbGDN2VWiPAP7rywabKhy8wb-9DXCHrc-gM7xDb5weM7x_rkfo-_lyfbZqLq8_X5wtLhvD5Lw0jA9CWlCauEHzuVUGpDTKdcIaOifOtUCEVsPAOBHOARDprKBdq3Qd2Tk7Qp-e7lbPf3aQSz_5bGAc6x_iLvdUdq3cP5tUqnqiVi85J3D9NvlJp7uekn5P6f_Lo4Kif8yj7n54ltkNE9h_my8BsAcjM42W</recordid><startdate>20150501</startdate><enddate>20150501</enddate><creator>Wang, Cheng</creator><creator>Luo, Zaiming</creator><creator>Kohan, Donald</creator><creator>Wellstein, Anton</creator><creator>Jose, Pedro A</creator><creator>Welch, William J</creator><creator>Wilcox, Christopher S</creator><creator>Wang, Dan</creator><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></search><sort><creationdate>20150501</creationdate><title>Thromboxane prostanoid receptors enhance contractions, endothelin-1, and oxidative stress in microvessels from mice with chronic kidney disease</title><author>Wang, Cheng ; Luo, Zaiming ; Kohan, Donald ; Wellstein, Anton ; Jose, Pedro A ; Welch, William J ; Wilcox, Christopher S ; Wang, Dan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c368t-34b56de9a0fba48d9ce66c9f75dc180ff2e05a9bb3405ffee06fd51729af2ed83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Arterioles - metabolism</topic><topic>Arterioles - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Endothelin-1 - biosynthesis</topic><topic>Endothelin-1 - genetics</topic><topic>Gene Expression Regulation</topic><topic>Kidney - blood supply</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Oxidative Stress</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Receptors, Thromboxane - biosynthesis</topic><topic>Receptors, Thromboxane - genetics</topic><topic>Renal Circulation</topic><topic>Renal Insufficiency, Chronic - genetics</topic><topic>Renal Insufficiency, Chronic - metabolism</topic><topic>Renal Insufficiency, Chronic - physiopathology</topic><topic>RNA - genetics</topic><topic>Vascular Remodeling</topic><topic>Vasoconstriction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Cheng</creatorcontrib><creatorcontrib>Luo, Zaiming</creatorcontrib><creatorcontrib>Kohan, Donald</creatorcontrib><creatorcontrib>Wellstein, Anton</creatorcontrib><creatorcontrib>Jose, Pedro A</creatorcontrib><creatorcontrib>Welch, William J</creatorcontrib><creatorcontrib>Wilcox, Christopher S</creatorcontrib><creatorcontrib>Wang, Dan</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>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Cheng</au><au>Luo, Zaiming</au><au>Kohan, Donald</au><au>Wellstein, Anton</au><au>Jose, Pedro A</au><au>Welch, William J</au><au>Wilcox, Christopher S</au><au>Wang, Dan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Thromboxane prostanoid receptors enhance contractions, endothelin-1, and oxidative stress in microvessels from mice with chronic kidney disease</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2015-05-01</date><risdate>2015</risdate><volume>65</volume><issue>5</issue><spage>1055</spage><epage>1063</epage><pages>1055-1063</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><abstract>Cardiovascular disease is frequent in chronic kidney disease and has been related to angiotensin II, endothelin-1 (ET-1), thromboxane A2, and reactive oxygen species (ROS). Because activation of thromboxane prostanoid receptors (TP-Rs) can generate ROS, which can generate ET-1, we tested the hypothesis that chronic kidney disease induces cyclooxygenase-2 whose products activate TP-Rs to enhance ET-1 and ROS generation and contractions. Mesenteric resistance arterioles were isolated from C57/BL6 or TP-R+/+ and TP-R-/- mice 3 months after SHAM-operation (SHAM) or surgical reduced renal mass (RRM, n=6/group). Microvascular contractions were studied on a wire myograph. Cellular (ethidium: dihydroethidium) and mitochondrial (mitoSOX) ROS were measured by fluorescence microscopy. Mice with RRM had increased excretion of markers of oxidative stress, thromboxane, and microalbumin; increased plasma ET-1; and increased microvascular expression of p22(phox), cyclooxygenase-2, TP-Rs, preproendothelin and endothelin-A receptors, and increased arteriolar remodeling. They had increased contractions to U-46,619 (118 ± 3 versus 87 ± 6, P<0.05) and ET-1 (108 ± 5 versus 89 ± 4, P<0.05), which were dependent on cellular and mitochondrial ROS, cyclooxygenase-2, and TP-Rs. RRM doubled the ET-1-induced cellular and mitochondrial ROS generation (P<0.05). TP-R-/- mice with RRM lacked these abnormal structural and functional microvascular responses and lacked the increased systemic and the increased microvascular oxidative stress and circulating ET-1. In conclusion, RRM leads to microvascular remodeling and enhanced ET-1-induced cellular and mitochondrial ROS and contractions that are mediated by cyclooxygenase-2 products activating TP-Rs. Thus, TP-Rs can be upstream from enhanced ROS, ET-1, microvascular remodeling, and contractility and may thereby coordinate vascular dysfunction in chronic kidney disease.</abstract><cop>United States</cop><pmid>25733239</pmid><doi>10.1161/HYPERTENSIONAHA.115.05244</doi><tpages>9</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 | Animals Arterioles - metabolism Arterioles - physiopathology Disease Models, Animal Endothelin-1 - biosynthesis Endothelin-1 - genetics Gene Expression Regulation Kidney - blood supply Male Mice Mice, Inbred C57BL Oxidative Stress Reactive Oxygen Species - metabolism Real-Time Polymerase Chain Reaction Receptors, Thromboxane - biosynthesis Receptors, Thromboxane - genetics Renal Circulation Renal Insufficiency, Chronic - genetics Renal Insufficiency, Chronic - metabolism Renal Insufficiency, Chronic - physiopathology RNA - genetics Vascular Remodeling Vasoconstriction |
| title | Thromboxane prostanoid receptors enhance contractions, endothelin-1, and oxidative stress in microvessels from mice with chronic kidney disease |
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