In vivo demonstration of H3‐histaminergic inhibition of cardiac sympathetic stimulation by R‐α‐methyl‐histamine and its prodrug BP 2.94 in the dog
The aim of this study was to investigate whether histamine H3‐receptor agonists could inhibit the effects of cardiac sympathetic nerve stimulation in the dog. Catecholamine release by the heart and the associated variation of haemodynamic parameters were measured after electrical stimulation of the...
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| Veröffentlicht in: | British journal of pharmacology 1999-01, Vol.126 (1), p.264-268 |
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| creator | Mazenot, Catherine Ribuot, Christophe Durand, Andrée Joulin, Yves Demenge, Pierre Godin‐Ribuot, Diane |
| description | The aim of this study was to investigate whether histamine H3‐receptor agonists could inhibit the effects of cardiac sympathetic nerve stimulation in the dog.
Catecholamine release by the heart and the associated variation of haemodynamic parameters were measured after electrical stimulation of the right cardiac sympathetic nerves (1–4 Hz, 10 V, 10 ms) in the anaesthetized dog treated with R‐α‐methyl‐histamine (R‐HA) and its prodrug BP 2.94 (BP).
Cardiac sympathetic stimulation induced a noradrenaline release into the coronary sinus along with a tachycardia and an increase in left ventricular pressure and contractility without changes in mean arterial pressure. Intravenous administration of H3‐receptor agonists significantly decreased noradrenaline release by the heart (R‐HA at 2 μmol kg−1 h−1: +77±25 vs +405±82; BP 2.94 at 1 mg kg−1: +12±11 vs +330±100 pg ml−1 in control conditions, P0.05), and increases in heart rate (R‐HA at 2 μmol kg−1 h−1: +26±8 vs +65±10 and BP 2.94 at 1 mg kg−1: +30±8 vs 75±6 beats min−1, in control conditions P0.05), left ventricular pressure, and contractility. Treatment with SC 359 (1 mg kg−1) a selective H3‐antagonist, reversed the effects of H3‐receptor agonists. Treatment with R‐HA at 2 μmol kg−1 h−1 and BP 2.94 at 1 mg kg−1 tended to decrease, while that with SC 359 significantly increased basal heart rate (from 111±3 to 130±5 beats min−1, P0.001).
Functional H3‐receptors are present on sympathetic nerve endings in the dog heart. Their stimulation by R‐α‐methyl‐histamine or BP 2.94 can inhibit noradrenaline release by the heart and its associated haemodynamic effects.
British Journal of Pharmacology (1999) 126, 264–268; doi:10.1038/sj.bjp.0702257 |
| doi_str_mv | 10.1038/sj.bjp.0702257 |
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Catecholamine release by the heart and the associated variation of haemodynamic parameters were measured after electrical stimulation of the right cardiac sympathetic nerves (1–4 Hz, 10 V, 10 ms) in the anaesthetized dog treated with R‐α‐methyl‐histamine (R‐HA) and its prodrug BP 2.94 (BP).
Cardiac sympathetic stimulation induced a noradrenaline release into the coronary sinus along with a tachycardia and an increase in left ventricular pressure and contractility without changes in mean arterial pressure. Intravenous administration of H3‐receptor agonists significantly decreased noradrenaline release by the heart (R‐HA at 2 μmol kg−1 h−1: +77±25 vs +405±82; BP 2.94 at 1 mg kg−1: +12±11 vs +330±100 pg ml−1 in control conditions, P0.05), and increases in heart rate (R‐HA at 2 μmol kg−1 h−1: +26±8 vs +65±10 and BP 2.94 at 1 mg kg−1: +30±8 vs 75±6 beats min−1, in control conditions P0.05), left ventricular pressure, and contractility. Treatment with SC 359 (1 mg kg−1) a selective H3‐antagonist, reversed the effects of H3‐receptor agonists. Treatment with R‐HA at 2 μmol kg−1 h−1 and BP 2.94 at 1 mg kg−1 tended to decrease, while that with SC 359 significantly increased basal heart rate (from 111±3 to 130±5 beats min−1, P0.001).
Functional H3‐receptors are present on sympathetic nerve endings in the dog heart. Their stimulation by R‐α‐methyl‐histamine or BP 2.94 can inhibit noradrenaline release by the heart and its associated haemodynamic effects.
British Journal of Pharmacology (1999) 126, 264–268; doi:10.1038/sj.bjp.0702257</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0702257</identifier><identifier>PMID: 10051144</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Biological and medical sciences ; Blood Pressure - drug effects ; BP 2.94 ; cardiac sympathetic nerves ; catecholamines ; Catecholamines - metabolism ; dog ; Dogs ; Dose-Response Relationship, Drug ; Electric Stimulation ; H3‐receptors ; Heart - drug effects ; Heart - innervation ; Heart Rate - drug effects ; Hemodynamics - drug effects ; Histamine Agonists - pharmacology ; Histamine Antagonists - pharmacology ; Imidazoles - pharmacology ; Imines - pharmacology ; Medical sciences ; Methylhistamines - pharmacology ; Miscellaneous ; Neuropharmacology ; Neurotransmitters. Neurotransmission. Receptors ; Pharmacology. Drug treatments ; Phenols - pharmacology ; Prodrugs - pharmacology ; Receptors, Histamine H3 - drug effects ; R‐α‐methyl‐histamine ; Sympathetic Nervous System - drug effects ; Sympathetic Nervous System - physiology ; Ventricular Function, Left - drug effects</subject><ispartof>British journal of pharmacology, 1999-01, Vol.126 (1), p.264-268</ispartof><rights>1999 Nature Publishing Group</rights><rights>1999 INIST-CNRS</rights><rights>Copyright 1999, Nature Publishing Group 1999 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1565770/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1565770/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,315,728,781,785,886,1418,1434,4025,27927,27928,27929,45578,45579,46413,46837,53795,53797</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1664314$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10051144$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mazenot, Catherine</creatorcontrib><creatorcontrib>Ribuot, Christophe</creatorcontrib><creatorcontrib>Durand, Andrée</creatorcontrib><creatorcontrib>Joulin, Yves</creatorcontrib><creatorcontrib>Demenge, Pierre</creatorcontrib><creatorcontrib>Godin‐Ribuot, Diane</creatorcontrib><title>In vivo demonstration of H3‐histaminergic inhibition of cardiac sympathetic stimulation by R‐α‐methyl‐histamine and its prodrug BP 2.94 in the dog</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>The aim of this study was to investigate whether histamine H3‐receptor agonists could inhibit the effects of cardiac sympathetic nerve stimulation in the dog.
Catecholamine release by the heart and the associated variation of haemodynamic parameters were measured after electrical stimulation of the right cardiac sympathetic nerves (1–4 Hz, 10 V, 10 ms) in the anaesthetized dog treated with R‐α‐methyl‐histamine (R‐HA) and its prodrug BP 2.94 (BP).
Cardiac sympathetic stimulation induced a noradrenaline release into the coronary sinus along with a tachycardia and an increase in left ventricular pressure and contractility without changes in mean arterial pressure. Intravenous administration of H3‐receptor agonists significantly decreased noradrenaline release by the heart (R‐HA at 2 μmol kg−1 h−1: +77±25 vs +405±82; BP 2.94 at 1 mg kg−1: +12±11 vs +330±100 pg ml−1 in control conditions, P0.05), and increases in heart rate (R‐HA at 2 μmol kg−1 h−1: +26±8 vs +65±10 and BP 2.94 at 1 mg kg−1: +30±8 vs 75±6 beats min−1, in control conditions P0.05), left ventricular pressure, and contractility. Treatment with SC 359 (1 mg kg−1) a selective H3‐antagonist, reversed the effects of H3‐receptor agonists. Treatment with R‐HA at 2 μmol kg−1 h−1 and BP 2.94 at 1 mg kg−1 tended to decrease, while that with SC 359 significantly increased basal heart rate (from 111±3 to 130±5 beats min−1, P0.001).
Functional H3‐receptors are present on sympathetic nerve endings in the dog heart. Their stimulation by R‐α‐methyl‐histamine or BP 2.94 can inhibit noradrenaline release by the heart and its associated haemodynamic effects.
British Journal of Pharmacology (1999) 126, 264–268; doi:10.1038/sj.bjp.0702257</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>BP 2.94</subject><subject>cardiac sympathetic nerves</subject><subject>catecholamines</subject><subject>Catecholamines - metabolism</subject><subject>dog</subject><subject>Dogs</subject><subject>Dose-Response Relationship, Drug</subject><subject>Electric Stimulation</subject><subject>H3‐receptors</subject><subject>Heart - drug effects</subject><subject>Heart - innervation</subject><subject>Heart Rate - drug effects</subject><subject>Hemodynamics - drug effects</subject><subject>Histamine Agonists - pharmacology</subject><subject>Histamine Antagonists - pharmacology</subject><subject>Imidazoles - pharmacology</subject><subject>Imines - pharmacology</subject><subject>Medical sciences</subject><subject>Methylhistamines - pharmacology</subject><subject>Miscellaneous</subject><subject>Neuropharmacology</subject><subject>Neurotransmitters. Neurotransmission. Receptors</subject><subject>Pharmacology. Drug treatments</subject><subject>Phenols - pharmacology</subject><subject>Prodrugs - pharmacology</subject><subject>Receptors, Histamine H3 - drug effects</subject><subject>R‐α‐methyl‐histamine</subject><subject>Sympathetic Nervous System - drug effects</subject><subject>Sympathetic Nervous System - physiology</subject><subject>Ventricular Function, Left - drug effects</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc9u1DAQhy0EokvhyhH5wDWL_9u5INGKspUqtargbNmOs_EqcaI4u1VuPAJ3nqIvwkPwJLjabdleZg7zzTfS_AB4j9ESI6o-pc3SboYlkogQLl-ABWZSFJwq_BIsEEKywFipE_AmpQ1CeSj5a3CCEeIYM7YAvy8j3IVdDyvf9TFNo5lCH2FfwxX9-_NXE9JkuhD9uA4OhtgEGx4BZ8YqGAfT3A1mavyUiTSFbtvuHXaGt1nx5z6Xzk_N3B4LoYkVDFOCw9hX43YNz24gWZYsH4FZBqt-_Ra8qk2b_LtDPwU_Lr5-P18VV9ffLs-_XBUDIZgWVlFJS1IrWzLhlPfY19LxuqyUNbWwRFDBBWOEGs4ochwb5wTljCiLuJf0FHzee4et7XzlfMxvaPUwhs6Ms-5N0M8nMTR63e805oJLibLgw7HgafPxzRn4eABMcqatRxNdSP85IRjFDxjZY3eh9fORRj9krdNG56z1IWt9drMqMaX_AOafpCY</recordid><startdate>199901</startdate><enddate>199901</enddate><creator>Mazenot, Catherine</creator><creator>Ribuot, Christophe</creator><creator>Durand, Andrée</creator><creator>Joulin, Yves</creator><creator>Demenge, Pierre</creator><creator>Godin‐Ribuot, Diane</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>5PM</scope></search><sort><creationdate>199901</creationdate><title>In vivo demonstration of H3‐histaminergic inhibition of cardiac sympathetic stimulation by R‐α‐methyl‐histamine and its prodrug BP 2.94 in the dog</title><author>Mazenot, Catherine ; Ribuot, Christophe ; Durand, Andrée ; Joulin, Yves ; Demenge, Pierre ; Godin‐Ribuot, Diane</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p2213-b837392f8b946c8ee1ef7c5f9d8baf6b2636564423a5430c51acc635428b05e73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>BP 2.94</topic><topic>cardiac sympathetic nerves</topic><topic>catecholamines</topic><topic>Catecholamines - metabolism</topic><topic>dog</topic><topic>Dogs</topic><topic>Dose-Response Relationship, Drug</topic><topic>Electric Stimulation</topic><topic>H3‐receptors</topic><topic>Heart - drug effects</topic><topic>Heart - innervation</topic><topic>Heart Rate - drug effects</topic><topic>Hemodynamics - drug effects</topic><topic>Histamine Agonists - pharmacology</topic><topic>Histamine Antagonists - pharmacology</topic><topic>Imidazoles - pharmacology</topic><topic>Imines - pharmacology</topic><topic>Medical sciences</topic><topic>Methylhistamines - pharmacology</topic><topic>Miscellaneous</topic><topic>Neuropharmacology</topic><topic>Neurotransmitters. Neurotransmission. Receptors</topic><topic>Pharmacology. Drug treatments</topic><topic>Phenols - pharmacology</topic><topic>Prodrugs - pharmacology</topic><topic>Receptors, Histamine H3 - drug effects</topic><topic>R‐α‐methyl‐histamine</topic><topic>Sympathetic Nervous System - drug effects</topic><topic>Sympathetic Nervous System - physiology</topic><topic>Ventricular Function, Left - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mazenot, Catherine</creatorcontrib><creatorcontrib>Ribuot, Christophe</creatorcontrib><creatorcontrib>Durand, Andrée</creatorcontrib><creatorcontrib>Joulin, Yves</creatorcontrib><creatorcontrib>Demenge, Pierre</creatorcontrib><creatorcontrib>Godin‐Ribuot, Diane</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>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mazenot, Catherine</au><au>Ribuot, Christophe</au><au>Durand, Andrée</au><au>Joulin, Yves</au><au>Demenge, Pierre</au><au>Godin‐Ribuot, Diane</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>In vivo demonstration of H3‐histaminergic inhibition of cardiac sympathetic stimulation by R‐α‐methyl‐histamine and its prodrug BP 2.94 in the dog</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>1999-01</date><risdate>1999</risdate><volume>126</volume><issue>1</issue><spage>264</spage><epage>268</epage><pages>264-268</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>The aim of this study was to investigate whether histamine H3‐receptor agonists could inhibit the effects of cardiac sympathetic nerve stimulation in the dog.
Catecholamine release by the heart and the associated variation of haemodynamic parameters were measured after electrical stimulation of the right cardiac sympathetic nerves (1–4 Hz, 10 V, 10 ms) in the anaesthetized dog treated with R‐α‐methyl‐histamine (R‐HA) and its prodrug BP 2.94 (BP).
Cardiac sympathetic stimulation induced a noradrenaline release into the coronary sinus along with a tachycardia and an increase in left ventricular pressure and contractility without changes in mean arterial pressure. Intravenous administration of H3‐receptor agonists significantly decreased noradrenaline release by the heart (R‐HA at 2 μmol kg−1 h−1: +77±25 vs +405±82; BP 2.94 at 1 mg kg−1: +12±11 vs +330±100 pg ml−1 in control conditions, P0.05), and increases in heart rate (R‐HA at 2 μmol kg−1 h−1: +26±8 vs +65±10 and BP 2.94 at 1 mg kg−1: +30±8 vs 75±6 beats min−1, in control conditions P0.05), left ventricular pressure, and contractility. Treatment with SC 359 (1 mg kg−1) a selective H3‐antagonist, reversed the effects of H3‐receptor agonists. Treatment with R‐HA at 2 μmol kg−1 h−1 and BP 2.94 at 1 mg kg−1 tended to decrease, while that with SC 359 significantly increased basal heart rate (from 111±3 to 130±5 beats min−1, P0.001).
Functional H3‐receptors are present on sympathetic nerve endings in the dog heart. Their stimulation by R‐α‐methyl‐histamine or BP 2.94 can inhibit noradrenaline release by the heart and its associated haemodynamic effects.
British Journal of Pharmacology (1999) 126, 264–268; doi:10.1038/sj.bjp.0702257</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>10051144</pmid><doi>10.1038/sj.bjp.0702257</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Blood Pressure - drug effects BP 2.94 cardiac sympathetic nerves catecholamines Catecholamines - metabolism dog Dogs Dose-Response Relationship, Drug Electric Stimulation H3‐receptors Heart - drug effects Heart - innervation Heart Rate - drug effects Hemodynamics - drug effects Histamine Agonists - pharmacology Histamine Antagonists - pharmacology Imidazoles - pharmacology Imines - pharmacology Medical sciences Methylhistamines - pharmacology Miscellaneous Neuropharmacology Neurotransmitters. Neurotransmission. Receptors Pharmacology. Drug treatments Phenols - pharmacology Prodrugs - pharmacology Receptors, Histamine H3 - drug effects R‐α‐methyl‐histamine Sympathetic Nervous System - drug effects Sympathetic Nervous System - physiology Ventricular Function, Left - drug effects |
| title | In vivo demonstration of H3‐histaminergic inhibition of cardiac sympathetic stimulation by R‐α‐methyl‐histamine and its prodrug BP 2.94 in the dog |
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