Contribution of Orexin to the Neurogenic Hypertension in BPH/2J Mice
BPH/2J mice are a genetic model of hypertension associated with an overactive sympathetic nervous system. Orexin is a neuropeptide which influences sympathetic activity and blood pressure. Orexin precursor mRNA expression is greater in hypothalamic tissue of BPH/2J compared with normotensive BPN/3J...
Gespeichert in:
| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2016-05, Vol.67 (5), p.959-969 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 969 |
|---|---|
| container_issue | 5 |
| container_start_page | 959 |
| container_title | Hypertension (Dallas, Tex. 1979) |
| container_volume | 67 |
| creator | Jackson, Kristy L Dampney, Bruno W Moretti, John-Luis Stevenson, Emily R Davern, Pamela J Carrive, Pascal Head, Geoffrey A |
| description | BPH/2J mice are a genetic model of hypertension associated with an overactive sympathetic nervous system. Orexin is a neuropeptide which influences sympathetic activity and blood pressure. Orexin precursor mRNA expression is greater in hypothalamic tissue of BPH/2J compared with normotensive BPN/3J mice. To determine whether enhanced orexinergic signaling contributes to the hypertension, BPH/2J and BPN/3J mice were preimplanted with radiotelemetry probes to compare blood pressure 1 hour before and 5 hours after administration of almorexant, an orexin receptor antagonist. Mid frequency mean arterial pressure power and the depressor response to ganglion blockade were also used as indicators of sympathetic nervous system activity. Administration of almorexant at 100 (IP) and 300 mg/kg (oral) in BPH/2J mice during the dark-active period (2 hours after lights off) markedly reduced blood pressure (−16.1±1.6 and −11.0±1.1 mm Hg, respectively; P |
| doi_str_mv | 10.1161/HYPERTENSIONAHA.115.07053 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1781539354</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1781539354</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4883-9fac5113acf5fc553fdc3f38e5bf97326fb4dae2695f00c53efcff874e3da6283</originalsourceid><addsrcrecordid>eNqNkE1PwkAQhjdGo4j-BVNvXgq73d1-HDwgosUgEMVET812OyvV0sXdNsi_twh68ORpkjfPOzN5EDonuEOIT7rxy3TwMBuMH4eTcS_uNSHv4ABzuodahHvMZdyn-6iFScTciJDnI3Rs7RvGhDEWHKIjz48CHuCoha77uqxMntZVrktHK2di4DMvnUo71RycMdRGv0KZSydeL8FUUNoN2BBX07jr3Tn3uYQTdKBEYeF0N9vo6WYw68fuaHI77PdGrmRhSN1ICckJoUIqriTnVGWSKhoCT1UUUM9XKcsENM9xhbHkFJRUKgwY0Ez4Xkjb6GK7d2n0Rw22Sha5lVAUogRd24QEIeE0opw1aLRFpdHWGlDJ0uQLYdYJwclGYvJHYhPy5Fti0z3bnanTBWS_zR9rDXC5BVa6qMDY96JegUnmIIpq_o8DXziYgvc</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1781539354</pqid></control><display><type>article</type><title>Contribution of Orexin to the Neurogenic Hypertension in BPH/2J Mice</title><source>MEDLINE</source><source>American Heart Association Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Journals@Ovid Complete</source><creator>Jackson, Kristy L ; Dampney, Bruno W ; Moretti, John-Luis ; Stevenson, Emily R ; Davern, Pamela J ; Carrive, Pascal ; Head, Geoffrey A</creator><creatorcontrib>Jackson, Kristy L ; Dampney, Bruno W ; Moretti, John-Luis ; Stevenson, Emily R ; Davern, Pamela J ; Carrive, Pascal ; Head, Geoffrey A</creatorcontrib><description>BPH/2J mice are a genetic model of hypertension associated with an overactive sympathetic nervous system. Orexin is a neuropeptide which influences sympathetic activity and blood pressure. Orexin precursor mRNA expression is greater in hypothalamic tissue of BPH/2J compared with normotensive BPN/3J mice. To determine whether enhanced orexinergic signaling contributes to the hypertension, BPH/2J and BPN/3J mice were preimplanted with radiotelemetry probes to compare blood pressure 1 hour before and 5 hours after administration of almorexant, an orexin receptor antagonist. Mid frequency mean arterial pressure power and the depressor response to ganglion blockade were also used as indicators of sympathetic nervous system activity. Administration of almorexant at 100 (IP) and 300 mg/kg (oral) in BPH/2J mice during the dark-active period (2 hours after lights off) markedly reduced blood pressure (−16.1±1.6 and −11.0±1.1 mm Hg, respectively; P<0.001 compared with vehicle). However, when almorexant (100 mg/kg, IP) was administered during the light-inactive period (5 hours before lights off) no reduction from baseline was observed (P=0.64). The same dose of almorexant in BPN/3J mice had no effect on blood pressure during the dark (P=0.79) or light periods (P=0.24). Almorexant attenuated the depressor response to ganglion blockade (P=0.018) and reduced the mid frequency mean arterial pressure power in BPH/2J mice (P<0.001), but not BPN/3J mice (P=0.70). Immunohistochemical labeling revealed that BPH/2J mice have 29% more orexin neurons than BPN/3J mice which are preferentially located in the lateral hypothalamus. The results suggest that enhanced orexinergic signaling contributes to sympathetic overactivity and hypertension during the dark period in BPH/2J mice.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/HYPERTENSIONAHA.115.07053</identifier><identifier>PMID: 26975709</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Acetamides - pharmacology ; Administration, Oral ; Animals ; Biomarkers - blood ; Blood Pressure Determination - methods ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Hypertension - drug therapy ; Hypertension - physiopathology ; Injections, Intraperitoneal ; Isoquinolines - pharmacology ; Male ; Mice ; Mice, Transgenic ; Motor Activity - drug effects ; Orexins - drug effects ; Orexins - metabolism ; Pressoreceptors - drug effects ; Pressoreceptors - physiology ; Random Allocation ; Reference Values ; Renin-Angiotensin System - drug effects ; Renin-Angiotensin System - physiology ; Sympathetic Nervous System - physiopathology ; Treatment Outcome</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2016-05, Vol.67 (5), p.959-969</ispartof><rights>2016 American Heart Association, Inc</rights><rights>2016 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4883-9fac5113acf5fc553fdc3f38e5bf97326fb4dae2695f00c53efcff874e3da6283</citedby><cites>FETCH-LOGICAL-c4883-9fac5113acf5fc553fdc3f38e5bf97326fb4dae2695f00c53efcff874e3da6283</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26975709$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jackson, Kristy L</creatorcontrib><creatorcontrib>Dampney, Bruno W</creatorcontrib><creatorcontrib>Moretti, John-Luis</creatorcontrib><creatorcontrib>Stevenson, Emily R</creatorcontrib><creatorcontrib>Davern, Pamela J</creatorcontrib><creatorcontrib>Carrive, Pascal</creatorcontrib><creatorcontrib>Head, Geoffrey A</creatorcontrib><title>Contribution of Orexin to the Neurogenic Hypertension in BPH/2J Mice</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>BPH/2J mice are a genetic model of hypertension associated with an overactive sympathetic nervous system. Orexin is a neuropeptide which influences sympathetic activity and blood pressure. Orexin precursor mRNA expression is greater in hypothalamic tissue of BPH/2J compared with normotensive BPN/3J mice. To determine whether enhanced orexinergic signaling contributes to the hypertension, BPH/2J and BPN/3J mice were preimplanted with radiotelemetry probes to compare blood pressure 1 hour before and 5 hours after administration of almorexant, an orexin receptor antagonist. Mid frequency mean arterial pressure power and the depressor response to ganglion blockade were also used as indicators of sympathetic nervous system activity. Administration of almorexant at 100 (IP) and 300 mg/kg (oral) in BPH/2J mice during the dark-active period (2 hours after lights off) markedly reduced blood pressure (−16.1±1.6 and −11.0±1.1 mm Hg, respectively; P<0.001 compared with vehicle). However, when almorexant (100 mg/kg, IP) was administered during the light-inactive period (5 hours before lights off) no reduction from baseline was observed (P=0.64). The same dose of almorexant in BPN/3J mice had no effect on blood pressure during the dark (P=0.79) or light periods (P=0.24). Almorexant attenuated the depressor response to ganglion blockade (P=0.018) and reduced the mid frequency mean arterial pressure power in BPH/2J mice (P<0.001), but not BPN/3J mice (P=0.70). Immunohistochemical labeling revealed that BPH/2J mice have 29% more orexin neurons than BPN/3J mice which are preferentially located in the lateral hypothalamus. The results suggest that enhanced orexinergic signaling contributes to sympathetic overactivity and hypertension during the dark period in BPH/2J mice.</description><subject>Acetamides - pharmacology</subject><subject>Administration, Oral</subject><subject>Animals</subject><subject>Biomarkers - blood</subject><subject>Blood Pressure Determination - methods</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - physiopathology</subject><subject>Injections, Intraperitoneal</subject><subject>Isoquinolines - pharmacology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Motor Activity - drug effects</subject><subject>Orexins - drug effects</subject><subject>Orexins - metabolism</subject><subject>Pressoreceptors - drug effects</subject><subject>Pressoreceptors - physiology</subject><subject>Random Allocation</subject><subject>Reference Values</subject><subject>Renin-Angiotensin System - drug effects</subject><subject>Renin-Angiotensin System - physiology</subject><subject>Sympathetic Nervous System - physiopathology</subject><subject>Treatment Outcome</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkE1PwkAQhjdGo4j-BVNvXgq73d1-HDwgosUgEMVET812OyvV0sXdNsi_twh68ORpkjfPOzN5EDonuEOIT7rxy3TwMBuMH4eTcS_uNSHv4ABzuodahHvMZdyn-6iFScTciJDnI3Rs7RvGhDEWHKIjz48CHuCoha77uqxMntZVrktHK2di4DMvnUo71RycMdRGv0KZSydeL8FUUNoN2BBX07jr3Tn3uYQTdKBEYeF0N9vo6WYw68fuaHI77PdGrmRhSN1ICckJoUIqriTnVGWSKhoCT1UUUM9XKcsENM9xhbHkFJRUKgwY0Ez4Xkjb6GK7d2n0Rw22Sha5lVAUogRd24QEIeE0opw1aLRFpdHWGlDJ0uQLYdYJwclGYvJHYhPy5Fti0z3bnanTBWS_zR9rDXC5BVa6qMDY96JegUnmIIpq_o8DXziYgvc</recordid><startdate>201605</startdate><enddate>201605</enddate><creator>Jackson, Kristy L</creator><creator>Dampney, Bruno W</creator><creator>Moretti, John-Luis</creator><creator>Stevenson, Emily R</creator><creator>Davern, Pamela J</creator><creator>Carrive, Pascal</creator><creator>Head, Geoffrey A</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></search><sort><creationdate>201605</creationdate><title>Contribution of Orexin to the Neurogenic Hypertension in BPH/2J Mice</title><author>Jackson, Kristy L ; Dampney, Bruno W ; Moretti, John-Luis ; Stevenson, Emily R ; Davern, Pamela J ; Carrive, Pascal ; Head, Geoffrey A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4883-9fac5113acf5fc553fdc3f38e5bf97326fb4dae2695f00c53efcff874e3da6283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Acetamides - pharmacology</topic><topic>Administration, Oral</topic><topic>Animals</topic><topic>Biomarkers - blood</topic><topic>Blood Pressure Determination - methods</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - physiopathology</topic><topic>Injections, Intraperitoneal</topic><topic>Isoquinolines - pharmacology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Motor Activity - drug effects</topic><topic>Orexins - drug effects</topic><topic>Orexins - metabolism</topic><topic>Pressoreceptors - drug effects</topic><topic>Pressoreceptors - physiology</topic><topic>Random Allocation</topic><topic>Reference Values</topic><topic>Renin-Angiotensin System - drug effects</topic><topic>Renin-Angiotensin System - physiology</topic><topic>Sympathetic Nervous System - physiopathology</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jackson, Kristy L</creatorcontrib><creatorcontrib>Dampney, Bruno W</creatorcontrib><creatorcontrib>Moretti, John-Luis</creatorcontrib><creatorcontrib>Stevenson, Emily R</creatorcontrib><creatorcontrib>Davern, Pamela J</creatorcontrib><creatorcontrib>Carrive, Pascal</creatorcontrib><creatorcontrib>Head, Geoffrey A</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>Jackson, Kristy L</au><au>Dampney, Bruno W</au><au>Moretti, John-Luis</au><au>Stevenson, Emily R</au><au>Davern, Pamela J</au><au>Carrive, Pascal</au><au>Head, Geoffrey A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Contribution of Orexin to the Neurogenic Hypertension in BPH/2J Mice</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2016-05</date><risdate>2016</risdate><volume>67</volume><issue>5</issue><spage>959</spage><epage>969</epage><pages>959-969</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><abstract>BPH/2J mice are a genetic model of hypertension associated with an overactive sympathetic nervous system. Orexin is a neuropeptide which influences sympathetic activity and blood pressure. Orexin precursor mRNA expression is greater in hypothalamic tissue of BPH/2J compared with normotensive BPN/3J mice. To determine whether enhanced orexinergic signaling contributes to the hypertension, BPH/2J and BPN/3J mice were preimplanted with radiotelemetry probes to compare blood pressure 1 hour before and 5 hours after administration of almorexant, an orexin receptor antagonist. Mid frequency mean arterial pressure power and the depressor response to ganglion blockade were also used as indicators of sympathetic nervous system activity. Administration of almorexant at 100 (IP) and 300 mg/kg (oral) in BPH/2J mice during the dark-active period (2 hours after lights off) markedly reduced blood pressure (−16.1±1.6 and −11.0±1.1 mm Hg, respectively; P<0.001 compared with vehicle). However, when almorexant (100 mg/kg, IP) was administered during the light-inactive period (5 hours before lights off) no reduction from baseline was observed (P=0.64). The same dose of almorexant in BPN/3J mice had no effect on blood pressure during the dark (P=0.79) or light periods (P=0.24). Almorexant attenuated the depressor response to ganglion blockade (P=0.018) and reduced the mid frequency mean arterial pressure power in BPH/2J mice (P<0.001), but not BPN/3J mice (P=0.70). Immunohistochemical labeling revealed that BPH/2J mice have 29% more orexin neurons than BPN/3J mice which are preferentially located in the lateral hypothalamus. The results suggest that enhanced orexinergic signaling contributes to sympathetic overactivity and hypertension during the dark period in BPH/2J mice.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>26975709</pmid><doi>10.1161/HYPERTENSIONAHA.115.07053</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0194-911X |
| ispartof | Hypertension (Dallas, Tex. 1979), 2016-05, Vol.67 (5), p.959-969 |
| issn | 0194-911X 1524-4563 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1781539354 |
| source | MEDLINE; American Heart Association Journals; EZB-FREE-00999 freely available EZB journals; Journals@Ovid Complete |
| subjects | Acetamides - pharmacology Administration, Oral Animals Biomarkers - blood Blood Pressure Determination - methods Disease Models, Animal Dose-Response Relationship, Drug Hypertension - drug therapy Hypertension - physiopathology Injections, Intraperitoneal Isoquinolines - pharmacology Male Mice Mice, Transgenic Motor Activity - drug effects Orexins - drug effects Orexins - metabolism Pressoreceptors - drug effects Pressoreceptors - physiology Random Allocation Reference Values Renin-Angiotensin System - drug effects Renin-Angiotensin System - physiology Sympathetic Nervous System - physiopathology Treatment Outcome |
| title | Contribution of Orexin to the Neurogenic Hypertension in BPH/2J Mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-31T23%3A41%3A22IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Contribution%20of%20Orexin%20to%20the%20Neurogenic%20Hypertension%20in%20BPH/2J%20Mice&rft.jtitle=Hypertension%20(Dallas,%20Tex.%201979)&rft.au=Jackson,%20Kristy%20L&rft.date=2016-05&rft.volume=67&rft.issue=5&rft.spage=959&rft.epage=969&rft.pages=959-969&rft.issn=0194-911X&rft.eissn=1524-4563&rft_id=info:doi/10.1161/HYPERTENSIONAHA.115.07053&rft_dat=%3Cproquest_cross%3E1781539354%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1781539354&rft_id=info:pmid/26975709&rfr_iscdi=true |