Activation of the central cholinergic system mediates the reversal of hypotension by centrally administrated U-46619, a thromboxane A2 analog, in hemorrhaged rats
In the present study, we investigated the role of the central cholinergic system in mediating the pressor effect of intracerebroventricularly administrated U-46619, a thromboxane A2 (TxA2) analog, in hemorrhaged hypotensive rats. Hemorrhage was performed by withdrawing a total volume of 2.1 ml of bl...
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description | In the present study, we investigated the role of the central cholinergic system in mediating the pressor effect of intracerebroventricularly administrated U-46619, a thromboxane A2 (TxA2) analog, in hemorrhaged hypotensive rats. Hemorrhage was performed by withdrawing a total volume of 2.1 ml of blood per 100 g body weight over a period of 10 min. Intracerebroventricular (i.c.v.) injection of U-46619 (0.5, 1, 2 μg) produced a dose- and time-dependent increase in arterial pressure and reversed the hypotension of this condition. Hemorrhage caused small increases in extracellular hypothalamic acetylcholine and choline levels. Intracerebroventricular administration of U-46619 (1 μg) further increased the levels of extracellular acetylcholine and choline by 57% and 41%, respectively. Pretreatment with SQ-29548 (8 μg; i.c.v.), a selective TxA2 receptor antagonist, completely abrogated the effects of subsequent injection of U-46619 (1 μg; i.c.v.) on arterial pressure and extracellular acetylcholine and choline levels. Pretreatment with mecamylamine (50 μg; i.c.v.), a cholinergic nonselective nicotinic receptor antagonist, attenuated the pressor effect of U-46619 (1 μg, i.c.v.) in hemorrhaged rats whereas pretreatment with atropine (10 μg; i.c.v.), a cholinergic nonselective muscarinic receptor antagonist, had no effect. Interestingly, pretreatment of rats with methyllycaconitine (10 μg; i.c.v.) or α-bungarotoxin (10 μg; i.c.v.), selective antagonists of α-7 subtype nicotinic acetylcholine receptors (α7nAChRs), partially abolished the pressor effect of U-46619 (1 μg; i.c.v.) in the hypotensive condition. Pretreatment with a combination of mecamylamine plus methyllycaconitine or mecamylamine plus α-bungarotoxin attenuated the reversal effect of U-46619, but only to the same extent as pretreatment with either antagonist alone. In conclusion, i.c.v. administration of U-46619 restores arterial pressure and increases posterior hypothalamic acetylcholine and choline levels by activating central TxA2 receptors in hemorrhaged hypotensive rats. The activation of central nicotinic cholinergic receptors, predominantly α7nAChRs, partially acts as a mediator in the pressor responses to i.c.v. injection of U-46619 under these conditions. |
doi_str_mv | 10.1016/j.brainres.2006.08.014 |
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Sertac ; Savci, Vahide</creator><creatorcontrib>Yalcin, Murat ; Cavun, Sinan ; Yilmaz, M. Sertac ; Savci, Vahide</creatorcontrib><description>In the present study, we investigated the role of the central cholinergic system in mediating the pressor effect of intracerebroventricularly administrated U-46619, a thromboxane A2 (TxA2) analog, in hemorrhaged hypotensive rats. Hemorrhage was performed by withdrawing a total volume of 2.1 ml of blood per 100 g body weight over a period of 10 min. Intracerebroventricular (i.c.v.) injection of U-46619 (0.5, 1, 2 μg) produced a dose- and time-dependent increase in arterial pressure and reversed the hypotension of this condition. Hemorrhage caused small increases in extracellular hypothalamic acetylcholine and choline levels. Intracerebroventricular administration of U-46619 (1 μg) further increased the levels of extracellular acetylcholine and choline by 57% and 41%, respectively. Pretreatment with SQ-29548 (8 μg; i.c.v.), a selective TxA2 receptor antagonist, completely abrogated the effects of subsequent injection of U-46619 (1 μg; i.c.v.) on arterial pressure and extracellular acetylcholine and choline levels. Pretreatment with mecamylamine (50 μg; i.c.v.), a cholinergic nonselective nicotinic receptor antagonist, attenuated the pressor effect of U-46619 (1 μg, i.c.v.) in hemorrhaged rats whereas pretreatment with atropine (10 μg; i.c.v.), a cholinergic nonselective muscarinic receptor antagonist, had no effect. Interestingly, pretreatment of rats with methyllycaconitine (10 μg; i.c.v.) or α-bungarotoxin (10 μg; i.c.v.), selective antagonists of α-7 subtype nicotinic acetylcholine receptors (α7nAChRs), partially abolished the pressor effect of U-46619 (1 μg; i.c.v.) in the hypotensive condition. Pretreatment with a combination of mecamylamine plus methyllycaconitine or mecamylamine plus α-bungarotoxin attenuated the reversal effect of U-46619, but only to the same extent as pretreatment with either antagonist alone. In conclusion, i.c.v. administration of U-46619 restores arterial pressure and increases posterior hypothalamic acetylcholine and choline levels by activating central TxA2 receptors in hemorrhaged hypotensive rats. The activation of central nicotinic cholinergic receptors, predominantly α7nAChRs, partially acts as a mediator in the pressor responses to i.c.v. injection of U-46619 under these conditions.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2006.08.014</identifier><identifier>PMID: 16962568</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology ; Acetylcholine - metabolism ; alpha7 Nicotinic Acetylcholine Receptor ; Animals ; Biological and medical sciences ; Blood Pressure - drug effects ; Blood Pressure - physiology ; Cholinergic ; Cholinergic Fibers - drug effects ; Cholinergic Fibers - metabolism ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Extracellular Fluid - drug effects ; Extracellular Fluid - metabolism ; Fundamental and applied biological sciences. Psychology ; Hemorrhage - complications ; Hemorrhage - physiopathology ; Hemorrhagic shock ; Hydrazines - pharmacology ; Hypotension - drug therapy ; Hypotension - etiology ; Hypotension - physiopathology ; Hypothalamus, Posterior - drug effects ; Hypothalamus, Posterior - metabolism ; Injections, Intraventricular ; Male ; Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration ; Neural Pathways - drug effects ; Neural Pathways - metabolism ; Nicotinic ; Nicotinic Antagonists - pharmacology ; Posterior hypothalamus ; Rats ; Rats, Sprague-Dawley ; Receptors, Nicotinic - drug effects ; Receptors, Nicotinic - metabolism ; Receptors, Thromboxane A2, Prostaglandin H2 - antagonists & inhibitors ; Receptors, Thromboxane A2, Prostaglandin H2 - metabolism ; Thromboxane A2 - analogs & derivatives ; Time Factors ; TxA2 ; Vasoconstrictor Agents - pharmacology ; Vertebrates: nervous system and sense organs ; α7nAChR</subject><ispartof>Brain research, 2006-11, Vol.1118 (1), p.43-51</ispartof><rights>2006 Elsevier B.V.</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-7ed1e22e29d63693c72bedc52ec8b0ae690ebd72a0aa638b981626d61182c2e03</citedby><cites>FETCH-LOGICAL-c427t-7ed1e22e29d63693c72bedc52ec8b0ae690ebd72a0aa638b981626d61182c2e03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.brainres.2006.08.014$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18255776$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16962568$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yalcin, Murat</creatorcontrib><creatorcontrib>Cavun, Sinan</creatorcontrib><creatorcontrib>Yilmaz, M. Sertac</creatorcontrib><creatorcontrib>Savci, Vahide</creatorcontrib><title>Activation of the central cholinergic system mediates the reversal of hypotension by centrally administrated U-46619, a thromboxane A2 analog, in hemorrhaged rats</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>In the present study, we investigated the role of the central cholinergic system in mediating the pressor effect of intracerebroventricularly administrated U-46619, a thromboxane A2 (TxA2) analog, in hemorrhaged hypotensive rats. Hemorrhage was performed by withdrawing a total volume of 2.1 ml of blood per 100 g body weight over a period of 10 min. Intracerebroventricular (i.c.v.) injection of U-46619 (0.5, 1, 2 μg) produced a dose- and time-dependent increase in arterial pressure and reversed the hypotension of this condition. Hemorrhage caused small increases in extracellular hypothalamic acetylcholine and choline levels. Intracerebroventricular administration of U-46619 (1 μg) further increased the levels of extracellular acetylcholine and choline by 57% and 41%, respectively. Pretreatment with SQ-29548 (8 μg; i.c.v.), a selective TxA2 receptor antagonist, completely abrogated the effects of subsequent injection of U-46619 (1 μg; i.c.v.) on arterial pressure and extracellular acetylcholine and choline levels. Pretreatment with mecamylamine (50 μg; i.c.v.), a cholinergic nonselective nicotinic receptor antagonist, attenuated the pressor effect of U-46619 (1 μg, i.c.v.) in hemorrhaged rats whereas pretreatment with atropine (10 μg; i.c.v.), a cholinergic nonselective muscarinic receptor antagonist, had no effect. Interestingly, pretreatment of rats with methyllycaconitine (10 μg; i.c.v.) or α-bungarotoxin (10 μg; i.c.v.), selective antagonists of α-7 subtype nicotinic acetylcholine receptors (α7nAChRs), partially abolished the pressor effect of U-46619 (1 μg; i.c.v.) in the hypotensive condition. Pretreatment with a combination of mecamylamine plus methyllycaconitine or mecamylamine plus α-bungarotoxin attenuated the reversal effect of U-46619, but only to the same extent as pretreatment with either antagonist alone. In conclusion, i.c.v. administration of U-46619 restores arterial pressure and increases posterior hypothalamic acetylcholine and choline levels by activating central TxA2 receptors in hemorrhaged hypotensive rats. The activation of central nicotinic cholinergic receptors, predominantly α7nAChRs, partially acts as a mediator in the pressor responses to i.c.v. injection of U-46619 under these conditions.</description><subject>15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology</subject><subject>Acetylcholine - metabolism</subject><subject>alpha7 Nicotinic Acetylcholine Receptor</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Pressure - physiology</subject><subject>Cholinergic</subject><subject>Cholinergic Fibers - drug effects</subject><subject>Cholinergic Fibers - metabolism</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Extracellular Fluid - drug effects</subject><subject>Extracellular Fluid - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hemorrhage - complications</subject><subject>Hemorrhage - physiopathology</subject><subject>Hemorrhagic shock</subject><subject>Hydrazines - pharmacology</subject><subject>Hypotension - drug therapy</subject><subject>Hypotension - etiology</subject><subject>Hypotension - physiopathology</subject><subject>Hypothalamus, Posterior - drug effects</subject><subject>Hypothalamus, Posterior - metabolism</subject><subject>Injections, Intraventricular</subject><subject>Male</subject><subject>Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration</subject><subject>Neural Pathways - drug effects</subject><subject>Neural Pathways - metabolism</subject><subject>Nicotinic</subject><subject>Nicotinic Antagonists - pharmacology</subject><subject>Posterior hypothalamus</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Nicotinic - drug effects</subject><subject>Receptors, Nicotinic - metabolism</subject><subject>Receptors, Thromboxane A2, Prostaglandin H2 - antagonists & inhibitors</subject><subject>Receptors, Thromboxane A2, Prostaglandin H2 - metabolism</subject><subject>Thromboxane A2 - analogs & derivatives</subject><subject>Time Factors</subject><subject>TxA2</subject><subject>Vasoconstrictor Agents - pharmacology</subject><subject>Vertebrates: nervous system and sense organs</subject><subject>α7nAChR</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1uGyEURlHVqnHTvkLEpl1lXGDGDOxqRf2TInXTrNEd5tqDNQMuYCvzOn3S4tpRllkhxPk-ru4h5IazJWdcft4tuwjOR0xLwZhcMrVkvHlFFly1opKiYa_JgpWXSmldX5F3Ke3Kta41e0uuuNRSrKRakL9rm90Rsguehg3NA1KLPkcYqR3C6DzGrbM0zSnjRCfsHWRM_7mIR4ypgCU3zPuQ0adTTTc_VYwzhX5y3qVyy9jTh6qRkutbCqUhhqkLj-CRrgUFD2PY3lLn6YBTiHGAbQmUWHpP3mxgTPjhcl6Th29ff9_9qO5_ff95t76vbCPaXLXYcxQChe5lLXVtW9Fhb1cCreoYoNQMu74VwABkrTqtuBSyl5wrYQWy-pp8OvfuY_hzwJTN5JLFcSwjhkMyUgneNs3LINe1Ei3nBZRn0MaQUsSN2Uc3QZwNZ-ak0ezMk0Zz0miYMkVjCd5cfjh0ZefPsYu3Any8AJAsjJsI3rr0zCmxWrWtLNyXM4dlcUeH0STr0NviMaLNpg_upVn-AXx0wVE</recordid><startdate>20061106</startdate><enddate>20061106</enddate><creator>Yalcin, Murat</creator><creator>Cavun, Sinan</creator><creator>Yilmaz, M. 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Sertac ; Savci, Vahide</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-7ed1e22e29d63693c72bedc52ec8b0ae690ebd72a0aa638b981626d61182c2e03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology</topic><topic>Acetylcholine - metabolism</topic><topic>alpha7 Nicotinic Acetylcholine Receptor</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Blood Pressure - physiology</topic><topic>Cholinergic</topic><topic>Cholinergic Fibers - drug effects</topic><topic>Cholinergic Fibers - metabolism</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Extracellular Fluid - drug effects</topic><topic>Extracellular Fluid - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hemorrhage - complications</topic><topic>Hemorrhage - physiopathology</topic><topic>Hemorrhagic shock</topic><topic>Hydrazines - pharmacology</topic><topic>Hypotension - drug therapy</topic><topic>Hypotension - etiology</topic><topic>Hypotension - physiopathology</topic><topic>Hypothalamus, Posterior - drug effects</topic><topic>Hypothalamus, Posterior - metabolism</topic><topic>Injections, Intraventricular</topic><topic>Male</topic><topic>Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration</topic><topic>Neural Pathways - drug effects</topic><topic>Neural Pathways - metabolism</topic><topic>Nicotinic</topic><topic>Nicotinic Antagonists - pharmacology</topic><topic>Posterior hypothalamus</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Nicotinic - drug effects</topic><topic>Receptors, Nicotinic - metabolism</topic><topic>Receptors, Thromboxane A2, Prostaglandin H2 - antagonists & inhibitors</topic><topic>Receptors, Thromboxane A2, Prostaglandin H2 - metabolism</topic><topic>Thromboxane A2 - analogs & derivatives</topic><topic>Time Factors</topic><topic>TxA2</topic><topic>Vasoconstrictor Agents - pharmacology</topic><topic>Vertebrates: nervous system and sense organs</topic><topic>α7nAChR</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yalcin, Murat</creatorcontrib><creatorcontrib>Cavun, Sinan</creatorcontrib><creatorcontrib>Yilmaz, M. Sertac</creatorcontrib><creatorcontrib>Savci, Vahide</creatorcontrib><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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yalcin, Murat</au><au>Cavun, Sinan</au><au>Yilmaz, M. Sertac</au><au>Savci, Vahide</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of the central cholinergic system mediates the reversal of hypotension by centrally administrated U-46619, a thromboxane A2 analog, in hemorrhaged rats</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2006-11-06</date><risdate>2006</risdate><volume>1118</volume><issue>1</issue><spage>43</spage><epage>51</epage><pages>43-51</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>In the present study, we investigated the role of the central cholinergic system in mediating the pressor effect of intracerebroventricularly administrated U-46619, a thromboxane A2 (TxA2) analog, in hemorrhaged hypotensive rats. Hemorrhage was performed by withdrawing a total volume of 2.1 ml of blood per 100 g body weight over a period of 10 min. Intracerebroventricular (i.c.v.) injection of U-46619 (0.5, 1, 2 μg) produced a dose- and time-dependent increase in arterial pressure and reversed the hypotension of this condition. Hemorrhage caused small increases in extracellular hypothalamic acetylcholine and choline levels. Intracerebroventricular administration of U-46619 (1 μg) further increased the levels of extracellular acetylcholine and choline by 57% and 41%, respectively. Pretreatment with SQ-29548 (8 μg; i.c.v.), a selective TxA2 receptor antagonist, completely abrogated the effects of subsequent injection of U-46619 (1 μg; i.c.v.) on arterial pressure and extracellular acetylcholine and choline levels. Pretreatment with mecamylamine (50 μg; i.c.v.), a cholinergic nonselective nicotinic receptor antagonist, attenuated the pressor effect of U-46619 (1 μg, i.c.v.) in hemorrhaged rats whereas pretreatment with atropine (10 μg; i.c.v.), a cholinergic nonselective muscarinic receptor antagonist, had no effect. Interestingly, pretreatment of rats with methyllycaconitine (10 μg; i.c.v.) or α-bungarotoxin (10 μg; i.c.v.), selective antagonists of α-7 subtype nicotinic acetylcholine receptors (α7nAChRs), partially abolished the pressor effect of U-46619 (1 μg; i.c.v.) in the hypotensive condition. Pretreatment with a combination of mecamylamine plus methyllycaconitine or mecamylamine plus α-bungarotoxin attenuated the reversal effect of U-46619, but only to the same extent as pretreatment with either antagonist alone. In conclusion, i.c.v. administration of U-46619 restores arterial pressure and increases posterior hypothalamic acetylcholine and choline levels by activating central TxA2 receptors in hemorrhaged hypotensive rats. The activation of central nicotinic cholinergic receptors, predominantly α7nAChRs, partially acts as a mediator in the pressor responses to i.c.v. injection of U-46619 under these conditions.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>16962568</pmid><doi>10.1016/j.brainres.2006.08.014</doi><tpages>9</tpages></addata></record> |
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subjects | 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid - pharmacology Acetylcholine - metabolism alpha7 Nicotinic Acetylcholine Receptor Animals Biological and medical sciences Blood Pressure - drug effects Blood Pressure - physiology Cholinergic Cholinergic Fibers - drug effects Cholinergic Fibers - metabolism Disease Models, Animal Dose-Response Relationship, Drug Extracellular Fluid - drug effects Extracellular Fluid - metabolism Fundamental and applied biological sciences. Psychology Hemorrhage - complications Hemorrhage - physiopathology Hemorrhagic shock Hydrazines - pharmacology Hypotension - drug therapy Hypotension - etiology Hypotension - physiopathology Hypothalamus, Posterior - drug effects Hypothalamus, Posterior - metabolism Injections, Intraventricular Male Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration Neural Pathways - drug effects Neural Pathways - metabolism Nicotinic Nicotinic Antagonists - pharmacology Posterior hypothalamus Rats Rats, Sprague-Dawley Receptors, Nicotinic - drug effects Receptors, Nicotinic - metabolism Receptors, Thromboxane A2, Prostaglandin H2 - antagonists & inhibitors Receptors, Thromboxane A2, Prostaglandin H2 - metabolism Thromboxane A2 - analogs & derivatives Time Factors TxA2 Vasoconstrictor Agents - pharmacology Vertebrates: nervous system and sense organs α7nAChR |
title | Activation of the central cholinergic system mediates the reversal of hypotension by centrally administrated U-46619, a thromboxane A2 analog, in hemorrhaged rats |
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