Differential cardiovascular effects of 8‐hydroxy‐2‐(di‐n‐propylamino) tetralin (8‐OH‐DPAT), flesinoxan, 5‐methyl‐urapidil and MDL 75,608A in conscious spontaneously hypertensive rats
Identifieur interne : 001E58 ( Istex/Corpus ); précédent : 001E57; suivant : 001E59Differential cardiovascular effects of 8‐hydroxy‐2‐(di‐n‐propylamino) tetralin (8‐OH‐DPAT), flesinoxan, 5‐methyl‐urapidil and MDL 75,608A in conscious spontaneously hypertensive rats
Auteurs : S. Buisson-Defferier ; M. Hibert ; M. Van Den BuuseSource :
- Fundamental & Clinical Pharmacology [ 0767-3981 ] ; 1993-12.
English descriptors
- KwdEn :
- Agonist, Anesthetized rats, Antihypertensive action, Arterial pressure, Basal, Basal blood pressures, Baseline values, Behavioural effects, Blood pressure, Bradycardia, Brain regions, Bruin receptors, Buuse, Cardiovascular, Cardiovascular effects, Cardiovascular response, Cardiovascular responses, Central receptors, Challenge dose, Chronic treatment, Conscious rats, Different doses, Dos, Flesinoxan, Fozard, Further experiments, Heart rate, Heart rate effects, High affinity, Hlood pressure, Hypertensive, Hypertensive rats, Hypotensive, Hypotensive action, Hypotensive effect, Hypotensive effects, Injection, Jugular vein, Little change, Mandal, Maximum effect, Mgkg, Moser, Nigkg, Normotensive, Normotensive rats, Other compounds, Other hand, Phenylephrine, Preliminary experiments, Present study, Pressor responses, Ramage, Rat, Receptor, Receptor agonists, Respective compounds, Saline injection, Saline injections, Significant difference, Such compounds, Tachycardia, Ventrolateral medulla, Wouters.
- Teeft :
- Agonist, Anesthetized rats, Antihypertensive action, Arterial pressure, Basal, Basal blood pressures, Baseline values, Behavioural effects, Blood pressure, Bradycardia, Brain regions, Bruin receptors, Buuse, Cardiovascular, Cardiovascular effects, Cardiovascular response, Cardiovascular responses, Central receptors, Challenge dose, Chronic treatment, Conscious rats, Different doses, Dos, Flesinoxan, Fozard, Further experiments, Heart rate, Heart rate effects, High affinity, Hlood pressure, Hypertensive, Hypertensive rats, Hypotensive, Hypotensive action, Hypotensive effect, Hypotensive effects, Injection, Jugular vein, Little change, Mandal, Maximum effect, Mgkg, Moser, Nigkg, Normotensive, Normotensive rats, Other compounds, Other hand, Phenylephrine, Preliminary experiments, Present study, Pressor responses, Ramage, Rat, Receptor, Receptor agonists, Respective compounds, Saline injection, Saline injections, Significant difference, Such compounds, Tachycardia, Ventrolateral medulla, Wouters.
Abstract
Summary— The effects of intravenous (iv) administration of four agonists at central 5‐HT1A receptors were investigated and compared. Acute iv injection of 0.1 mg/kg of 8‐OH‐DPAT induced a decrease in blood pressure both in spontaneously hypertensive rats (SHR) and normotensive Wistar‐Kyoto rats (WKY). The maximal hypotensive effect was observed 15 and 10 min after injection, respectively, but the effect was greater and longer‐lasting in the SHR. 8‐OH‐DPAT significantly decreased heart rate in WKY and, to a lesser extent, in SHR. The iv injection of 1 mg/kg of flesinoxan caused a similar fall in blood pressure and heart rate in SHR and WKY. The iv administration of 1 mg/kg of 5‐methyl‐urapidil or MDL 75,608A caused a fall in blood pressure which was significantly more pronounced in SHR than in WKY. 5‐methyl‐urapidil induced a significant tachycardia in WKY, but had little effect on heart rate in SHR. MDL 75,608A caused a short‐lasting tachycardia in SHR and WKY. In conscious SHR, the intracerebroventricular (icv) injection of 10 μg of 8‐OH‐DPAT or 100 μg of either flesinoxan or MDL 75,608A caused a decrease in blood pressure and heart rate. The icv injection of 100 μg of 5‐methyl‐urapidil caused only a decrease in blood pressure. Chronic pre‐treatment with these compounds, by daily iv injection, did not significantly influence the hypotensive or bradycardic effects in an acute experiment. The involvement of α1‐adrenoceptors in the effects of these compounds was studied by administering phenylephrine (1 μg/iv) at 5‐ min intervals before and after the iv injection of the experimental compounds. The injection of phenylephrine reproducibly increased blood pressure by 35–40 mm Hg after saline pre‐treatment, and these responses were not affected by the iv injection of 0.1 mg/kg of either 8‐OH‐DPAT or 1 mg/kg of flesinoxan. In contrast, the phenylephrine‐induced pressor responses were markedly diminished at 5 min after treatment with 1 mg/kg of either 5‐methyl‐urapidil or MDL 75,608A, but slowly recovered thereafter. These results show that the 5‐HT1A recptor agonists 8‐OH‐DPAT, flesinoxan, 5‐methyl‐urapidil and MDL 75,608A show antihypertensive properties in conscious SHR after iv or icv injection. However, the mechanism of action of the compounds differs: 8‐OH‐DPAT and flesinoxan may act predominantly as 5‐HT1A receptor agonists, where as 5‐methyl‐urapidil and MDL 75,608A also seem to have an effect on peripheral α1‐adrenoceptors.
Url:
DOI: 10.1111/j.1472-8206.1993.tb00254.x
Links to Exploration step
ISTEX:A1844558F0EE050164323A09CA7B0F18556CCAC9Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Differential cardiovascular effects of 8‐hydroxy‐2‐(di‐n‐propylamino) tetralin (8‐OH‐DPAT), flesinoxan, 5‐methyl‐urapidil and MDL 75,608A in conscious spontaneously hypertensive rats</title><author><name sortKey="Buisson Efferier, S" sort="Buisson Efferier, S" uniqKey="Buisson Efferier S" first="S." last="Buisson-Defferier">S. Buisson-Defferier</name><affiliation><mods:affiliation>Marion Merrell Dow Research Institute, Strasbourg Research Center, 16, rue d'Ankara, BP 067, 67046 Strasbourg Cedex, France</mods:affiliation></affiliation></author><author><name sortKey="Hibert, M" sort="Hibert, M" uniqKey="Hibert M" first="M." last="Hibert">M. Hibert</name><affiliation><mods:affiliation>Marion Merrell Dow Research Institute, Strasbourg Research Center, 16, rue d'Ankara, BP 067, 67046 Strasbourg Cedex, France</mods:affiliation></affiliation></author><author><name sortKey="Van Den Buuse, M" sort="Van Den Buuse, M" uniqKey="Van Den Buuse M" first="M." last="Van Den Buuse">M. Van Den Buuse</name><affiliation><mods:affiliation>Baker Medical Research Institute, Conunercial Road, PO Box 348, Prahran, Vic 3181, Australia</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:A1844558F0EE050164323A09CA7B0F18556CCAC9</idno><date when="1993" year="1993">1993</date><idno type="doi">10.1111/j.1472-8206.1993.tb00254.x</idno><idno type="url">https://api.istex.fr/document/A1844558F0EE050164323A09CA7B0F18556CCAC9/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001E58</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001E58</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Differential cardiovascular effects of 8‐hydroxy‐2‐(di‐n‐propylamino) tetralin (8‐OH‐DPAT), flesinoxan, 5‐methyl‐urapidil and MDL 75,608A in conscious spontaneously hypertensive rats</title><author><name sortKey="Buisson Efferier, S" sort="Buisson Efferier, S" uniqKey="Buisson Efferier S" first="S." last="Buisson-Defferier">S. Buisson-Defferier</name><affiliation><mods:affiliation>Marion Merrell Dow Research Institute, Strasbourg Research Center, 16, rue d'Ankara, BP 067, 67046 Strasbourg Cedex, France</mods:affiliation></affiliation></author><author><name sortKey="Hibert, M" sort="Hibert, M" uniqKey="Hibert M" first="M." last="Hibert">M. Hibert</name><affiliation><mods:affiliation>Marion Merrell Dow Research Institute, Strasbourg Research Center, 16, rue d'Ankara, BP 067, 67046 Strasbourg Cedex, France</mods:affiliation></affiliation></author><author><name sortKey="Van Den Buuse, M" sort="Van Den Buuse, M" uniqKey="Van Den Buuse M" first="M." last="Van Den Buuse">M. Van Den Buuse</name><affiliation><mods:affiliation>Baker Medical Research Institute, Conunercial Road, PO Box 348, Prahran, Vic 3181, Australia</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Fundamental & Clinical Pharmacology</title><title level="j" type="alt">FUNDAMENTAL CLINICAL PHARMACOLOGY</title><idno type="ISSN">0767-3981</idno><idno type="eISSN">1472-8206</idno><imprint><biblScope unit="vol">7</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="499">499</biblScope><biblScope unit="page" to="511">511</biblScope><biblScope unit="page-count">13</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1993-12">1993-12</date></imprint><idno type="ISSN">0767-3981</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0767-3981</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Agonist</term><term>Anesthetized rats</term><term>Antihypertensive action</term><term>Arterial pressure</term><term>Basal</term><term>Basal blood pressures</term><term>Baseline values</term><term>Behavioural effects</term><term>Blood pressure</term><term>Bradycardia</term><term>Brain regions</term><term>Bruin receptors</term><term>Buuse</term><term>Cardiovascular</term><term>Cardiovascular effects</term><term>Cardiovascular response</term><term>Cardiovascular responses</term><term>Central receptors</term><term>Challenge dose</term><term>Chronic treatment</term><term>Conscious rats</term><term>Different doses</term><term>Dos</term><term>Flesinoxan</term><term>Fozard</term><term>Further experiments</term><term>Heart rate</term><term>Heart rate effects</term><term>High affinity</term><term>Hlood pressure</term><term>Hypertensive</term><term>Hypertensive rats</term><term>Hypotensive</term><term>Hypotensive action</term><term>Hypotensive effect</term><term>Hypotensive effects</term><term>Injection</term><term>Jugular vein</term><term>Little change</term><term>Mandal</term><term>Maximum effect</term><term>Mgkg</term><term>Moser</term><term>Nigkg</term><term>Normotensive</term><term>Normotensive rats</term><term>Other compounds</term><term>Other hand</term><term>Phenylephrine</term><term>Preliminary experiments</term><term>Present study</term><term>Pressor responses</term><term>Ramage</term><term>Rat</term><term>Receptor</term><term>Receptor agonists</term><term>Respective compounds</term><term>Saline injection</term><term>Saline injections</term><term>Significant difference</term><term>Such compounds</term><term>Tachycardia</term><term>Ventrolateral medulla</term><term>Wouters</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Agonist</term><term>Anesthetized rats</term><term>Antihypertensive action</term><term>Arterial pressure</term><term>Basal</term><term>Basal blood pressures</term><term>Baseline values</term><term>Behavioural effects</term><term>Blood pressure</term><term>Bradycardia</term><term>Brain regions</term><term>Bruin receptors</term><term>Buuse</term><term>Cardiovascular</term><term>Cardiovascular effects</term><term>Cardiovascular response</term><term>Cardiovascular responses</term><term>Central receptors</term><term>Challenge dose</term><term>Chronic treatment</term><term>Conscious rats</term><term>Different doses</term><term>Dos</term><term>Flesinoxan</term><term>Fozard</term><term>Further experiments</term><term>Heart rate</term><term>Heart rate effects</term><term>High affinity</term><term>Hlood pressure</term><term>Hypertensive</term><term>Hypertensive rats</term><term>Hypotensive</term><term>Hypotensive action</term><term>Hypotensive effect</term><term>Hypotensive effects</term><term>Injection</term><term>Jugular vein</term><term>Little change</term><term>Mandal</term><term>Maximum effect</term><term>Mgkg</term><term>Moser</term><term>Nigkg</term><term>Normotensive</term><term>Normotensive rats</term><term>Other compounds</term><term>Other hand</term><term>Phenylephrine</term><term>Preliminary experiments</term><term>Present study</term><term>Pressor responses</term><term>Ramage</term><term>Rat</term><term>Receptor</term><term>Receptor agonists</term><term>Respective compounds</term><term>Saline injection</term><term>Saline injections</term><term>Significant difference</term><term>Such compounds</term><term>Tachycardia</term><term>Ventrolateral medulla</term><term>Wouters</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract">Summary— The effects of intravenous (iv) administration of four agonists at central 5‐HT1A receptors were investigated and compared. Acute iv injection of 0.1 mg/kg of 8‐OH‐DPAT induced a decrease in blood pressure both in spontaneously hypertensive rats (SHR) and normotensive Wistar‐Kyoto rats (WKY). The maximal hypotensive effect was observed 15 and 10 min after injection, respectively, but the effect was greater and longer‐lasting in the SHR. 8‐OH‐DPAT significantly decreased heart rate in WKY and, to a lesser extent, in SHR. The iv injection of 1 mg/kg of flesinoxan caused a similar fall in blood pressure and heart rate in SHR and WKY. The iv administration of 1 mg/kg of 5‐methyl‐urapidil or MDL 75,608A caused a fall in blood pressure which was significantly more pronounced in SHR than in WKY. 5‐methyl‐urapidil induced a significant tachycardia in WKY, but had little effect on heart rate in SHR. MDL 75,608A caused a short‐lasting tachycardia in SHR and WKY. In conscious SHR, the intracerebroventricular (icv) injection of 10 μg of 8‐OH‐DPAT or 100 μg of either flesinoxan or MDL 75,608A caused a decrease in blood pressure and heart rate. The icv injection of 100 μg of 5‐methyl‐urapidil caused only a decrease in blood pressure. Chronic pre‐treatment with these compounds, by daily iv injection, did not significantly influence the hypotensive or bradycardic effects in an acute experiment. The involvement of α1‐adrenoceptors in the effects of these compounds was studied by administering phenylephrine (1 μg/iv) at 5‐ min intervals before and after the iv injection of the experimental compounds. The injection of phenylephrine reproducibly increased blood pressure by 35–40 mm Hg after saline pre‐treatment, and these responses were not affected by the iv injection of 0.1 mg/kg of either 8‐OH‐DPAT or 1 mg/kg of flesinoxan. In contrast, the phenylephrine‐induced pressor responses were markedly diminished at 5 min after treatment with 1 mg/kg of either 5‐methyl‐urapidil or MDL 75,608A, but slowly recovered thereafter. These results show that the 5‐HT1A recptor agonists 8‐OH‐DPAT, flesinoxan, 5‐methyl‐urapidil and MDL 75,608A show antihypertensive properties in conscious SHR after iv or icv injection. However, the mechanism of action of the compounds differs: 8‐OH‐DPAT and flesinoxan may act predominantly as 5‐HT1A receptor agonists, where as 5‐methyl‐urapidil and MDL 75,608A also seem to have an effect on peripheral α1‐adrenoceptors.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>flesinoxan</json:string><json:string>receptor</json:string><json:string>blood pressure</json:string><json:string>heart rate</json:string><json:string>agonist</json:string><json:string>bradycardia</json:string><json:string>hypotensive</json:string><json:string>hypertensive</json:string><json:string>wouters</json:string><json:string>fozard</json:string><json:string>tachycardia</json:string><json:string>central receptors</json:string><json:string>ramage</json:string><json:string>basal</json:string><json:string>hypertensive rats</json:string><json:string>phenylephrine</json:string><json:string>normotensive</json:string><json:string>mgkg</json:string><json:string>nigkg</json:string><json:string>buuse</json:string><json:string>moser</json:string><json:string>mandal</json:string><json:string>cardiovascular</json:string><json:string>cardiovascular effects</json:string><json:string>other compounds</json:string><json:string>arterial pressure</json:string><json:string>high affinity</json:string><json:string>dos</json:string><json:string>hlood pressure</json:string><json:string>injection</json:string><json:string>hypotensive effect</json:string><json:string>different doses</json:string><json:string>hypotensive action</json:string><json:string>heart rate effects</json:string><json:string>saline injections</json:string><json:string>behavioural effects</json:string><json:string>preliminary experiments</json:string><json:string>significant difference</json:string><json:string>receptor agonists</json:string><json:string>rat</json:string><json:string>brain regions</json:string><json:string>chronic treatment</json:string><json:string>present study</json:string><json:string>baseline values</json:string><json:string>little change</json:string><json:string>such compounds</json:string><json:string>further experiments</json:string><json:string>maximum effect</json:string><json:string>ventrolateral medulla</json:string><json:string>basal blood pressures</json:string><json:string>bruin receptors</json:string><json:string>challenge dose</json:string><json:string>saline injection</json:string><json:string>respective compounds</json:string><json:string>pressor responses</json:string><json:string>conscious rats</json:string><json:string>antihypertensive action</json:string><json:string>anesthetized rats</json:string><json:string>normotensive rats</json:string><json:string>cardiovascular response</json:string><json:string>cardiovascular responses</json:string><json:string>other hand</json:string><json:string>hypotensive effects</json:string><json:string>jugular vein</json:string></teeft></keywords><author><json:item><name>S. Buisson‐Defferier</name><affiliations><json:string>Marion Merrell Dow Research Institute, Strasbourg Research Center, 16, rue d'Ankara, BP 067, 67046 Strasbourg Cedex, France</json:string></affiliations></json:item><json:item><name>M. Hibert</name><affiliations><json:string>Marion Merrell Dow Research Institute, Strasbourg Research Center, 16, rue d'Ankara, BP 067, 67046 Strasbourg Cedex, France</json:string></affiliations></json:item><json:item><name>M. van den Buuse</name><affiliations><json:string>Baker Medical Research Institute, Conunercial Road, PO Box 348, Prahran, Vic 3181, Australia</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>serotonin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>5‐HT1A‐receptor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>blood pressure</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>heart rate</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>spontaneously hypertensive rat</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>desensitization</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>α1‐adrenoceptor</value></json:item></subject><articleId><json:string>FCP254</json:string></articleId><arkIstex>ark:/67375/WNG-7LXHFB56-W</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Summary— The effects of intravenous (iv) administration of four agonists at central 5‐HT1A receptors were investigated and compared. Acute iv injection of 0.1 mg/kg of 8‐OH‐DPAT induced a decrease in blood pressure both in spontaneously hypertensive rats (SHR) and normotensive Wistar‐Kyoto rats (WKY). The maximal hypotensive effect was observed 15 and 10 min after injection, respectively, but the effect was greater and longer‐lasting in the SHR. 8‐OH‐DPAT significantly decreased heart rate in WKY and, to a lesser extent, in SHR. The iv injection of 1 mg/kg of flesinoxan caused a similar fall in blood pressure and heart rate in SHR and WKY. The iv administration of 1 mg/kg of 5‐methyl‐urapidil or MDL 75,608A caused a fall in blood pressure which was significantly more pronounced in SHR than in WKY. 5‐methyl‐urapidil induced a significant tachycardia in WKY, but had little effect on heart rate in SHR. MDL 75,608A caused a short‐lasting tachycardia in SHR and WKY. In conscious SHR, the intracerebroventricular (icv) injection of 10 μg of 8‐OH‐DPAT or 100 μg of either flesinoxan or MDL 75,608A caused a decrease in blood pressure and heart rate. The icv injection of 100 μg of 5‐methyl‐urapidil caused only a decrease in blood pressure. Chronic pre‐treatment with these compounds, by daily iv injection, did not significantly influence the hypotensive or bradycardic effects in an acute experiment. The involvement of α1‐adrenoceptors in the effects of these compounds was studied by administering phenylephrine (1 μg/iv) at 5‐ min intervals before and after the iv injection of the experimental compounds. The injection of phenylephrine reproducibly increased blood pressure by 35–40 mm Hg after saline pre‐treatment, and these responses were not affected by the iv injection of 0.1 mg/kg of either 8‐OH‐DPAT or 1 mg/kg of flesinoxan. In contrast, the phenylephrine‐induced pressor responses were markedly diminished at 5 min after treatment with 1 mg/kg of either 5‐methyl‐urapidil or MDL 75,608A, but slowly recovered thereafter. These results show that the 5‐HT1A recptor agonists 8‐OH‐DPAT, flesinoxan, 5‐methyl‐urapidil and MDL 75,608A show antihypertensive properties in conscious SHR after iv or icv injection. However, the mechanism of action of the compounds differs: 8‐OH‐DPAT and flesinoxan may act predominantly as 5‐HT1A receptor agonists, where as 5‐methyl‐urapidil and MDL 75,608A also seem to have an effect on peripheral α1‐adrenoceptors.</abstract><qualityIndicators><score>10</score><pdfWordCount>5595</pdfWordCount><pdfCharCount>33938</pdfCharCount><pdfVersion>1.4</pdfVersion><pdfPageCount>13</pdfPageCount><pdfPageSize>540 x 756 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>375</abstractWordCount><abstractCharCount>2468</abstractCharCount><keywordCount>7</keywordCount></qualityIndicators><title>Differential cardiovascular effects of 8‐hydroxy‐2‐(di‐n‐propylamino) tetralin (8‐OH‐DPAT), flesinoxan, 5‐methyl‐urapidil and MDL 75,608A in conscious spontaneously hypertensive rats</title><pmid><json:string>7906241</json:string></pmid><genre><json:string>article</json:string></genre><host><title>Fundamental & Clinical Pharmacology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1472-8206</json:string></doi><issn><json:string>0767-3981</json:string></issn><eissn><json:string>1472-8206</json:string></eissn><publisherId><json:string>FCP</json:string></publisherId><volume>7</volume><issue>9</issue><pages><first>499</first><last>511</last><total>13</total></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1993</json:string></date><geogName></geogName><orgName><json:string>Research Biochcmicals</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Irene Fornieles</json:string></persName><placeName><json:string>Kyoto</json:string><json:string>Israel</json:string><json:string>France</json:string><json:string>Netherlands</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Middlemiss and Fozard, 1983</json:string><json:string>Moser, 1991</json:string><json:string>Sanders et al, 1990</json:string><json:string>Buisson-Defferier and Van den Buuse, 1992</json:string><json:string>Gross et crl, 1990</json:string><json:string>Doods et al, 1988</json:string><json:string>Wouters et al, 1988b</json:string><json:string>Kolbasa et al, 1991</json:string><json:string>Palacios et al, 1987</json:string><json:string>Mandal et nl, 1990</json:string><json:string>Kubo et nl, 1990</json:string><json:string>Moser et al, 1990</json:string><json:string>Fozard er ut, 1987</json:string><json:string>Van Wijngaarden et al, 1990</json:string><json:string>Wouters et al, 1988a</json:string><json:string>Van den Buuse, 1992</json:string><json:string>Varrault et ol, 1991</json:string><json:string>Valenta and Singer, 1990</json:string><json:string>Head and Adams, 1992</json:string><json:string>Ramage and Wilkinson, 1989</json:string><json:string>Kuhn et el, 1980</json:string><json:string>Blier and De Montigny, 1987</json:string><json:string>Martin and Lis, 1985</json:string><json:string>Van Wijngaarden et af, 1990</json:string><json:string>Kreiss and Lucki, 1992</json:string><json:string>Gilbert et al, 1988</json:string><json:string>Gross et al, 1990</json:string><json:string>Ramage, 1990</json:string><json:string>Koulu ef d , 1986</json:string><json:string>Van Wijngaarden er nl, 1990</json:string><json:string>Mandal et d, 1991</json:string><json:string>Felten el nl, 1984</json:string><json:string>Buisson-Dcfferier and Van den Buuse, 1992</json:string><json:string>Wouters et crl, 1988a</json:string><json:string>Manaker and Verderanie, 1990</json:string><json:string>Gross e( ril, 1990</json:string><json:string>Kennctt et al, 1987</json:string><json:string>Gradin el d , 1985</json:string><json:string>Huguet and Brisac, 1991</json:string><json:string>Ramage, 1988</json:string><json:string>Mir and Fozard, 1987</json:string><json:string>Kellar et al, 1991</json:string><json:string>Bottiglieri et (11, 1988</json:string><json:string>Gradin et al, 1985</json:string><json:string>Larsson et nl, 1990</json:string><json:string>Mandal et al, 1990</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/WNG-7LXHFB56-W</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - pharmacology & pharmacy</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - pharmacology & pharmacy</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Pharmacology (medical)</json:string><json:string>1 - Life Sciences</json:string><json:string>2 - Pharmacology, Toxicology and Pharmaceutics</json:string><json:string>3 - Pharmacology</json:string></scopus></categories><publicationDate>1993</publicationDate><copyrightDate>1993</copyrightDate><doi><json:string>10.1111/j.1472-8206.1993.tb00254.x</json:string></doi><id>A1844558F0EE050164323A09CA7B0F18556CCAC9</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/A1844558F0EE050164323A09CA7B0F18556CCAC9/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/A1844558F0EE050164323A09CA7B0F18556CCAC9/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/A1844558F0EE050164323A09CA7B0F18556CCAC9/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">Differential cardiovascular effects of 8‐hydroxy‐2‐(di‐n‐propylamino) tetralin (8‐OH‐DPAT), flesinoxan, 5‐methyl‐urapidil and MDL 75,608A in conscious spontaneously hypertensive rats</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><licence>1993 Société Française de Pharmacologie et de Thérapeutique</licence></availability><date type="published" when="1993-12"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Differential cardiovascular effects of 8‐hydroxy‐2‐(di‐n‐propylamino) tetralin (8‐OH‐DPAT), flesinoxan, 5‐methyl‐urapidil and MDL 75,608A in conscious spontaneously hypertensive rats</title><author xml:id="author-0000"><persName><forename type="first">S.</forename><surname>Buisson‐Defferier</surname></persName><affiliation>Marion Merrell Dow Research Institute, Strasbourg Research Center, 16, rue d'Ankara, BP 067, 67046 Strasbourg Cedex, France<address><country key="FR"></country></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">M.</forename><surname>Hibert</surname></persName><affiliation>Marion Merrell Dow Research Institute, Strasbourg Research Center, 16, rue d'Ankara, BP 067, 67046 Strasbourg Cedex, France<address><country key="FR"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">M.</forename><surname>Buuse</surname></persName><affiliation>Baker Medical Research Institute, Conunercial Road, PO Box 348, Prahran, Vic 3181, Australia<address><country key="AU"></country></address></affiliation></author><idno type="istex">A1844558F0EE050164323A09CA7B0F18556CCAC9</idno><idno type="ark">ark:/67375/WNG-7LXHFB56-W</idno><idno type="DOI">10.1111/j.1472-8206.1993.tb00254.x</idno><idno type="unit">FCP254</idno><idno type="toTypesetVersion">file:FCP.FCP254.pdf</idno></analytic><monogr><title level="j" type="main">Fundamental & Clinical Pharmacology</title><title level="j" type="alt">FUNDAMENTAL CLINICAL PHARMACOLOGY</title><idno type="pISSN">0767-3981</idno><idno type="eISSN">1472-8206</idno><idno type="book-DOI">10.1111/(ISSN)1472-8206</idno><idno type="book-part-DOI">10.1111/fcp.1993.7.issue-9</idno><idno type="product">FCP</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">7</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="499">499</biblScope><biblScope unit="page" to="511">511</biblScope><biblScope unit="page-count">13</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1993-12"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p><hi rend="bold">Summary—</hi> The effects of intravenous (iv) administration of four agonists at central 5‐HT<hi rend="subscript">1A</hi> receptors were investigated and compared. Acute iv injection of 0.1 mg/kg of 8‐OH‐DPAT induced a decrease in blood pressure both in spontaneously hypertensive rats (SHR) and normotensive Wistar‐Kyoto rats (WKY). The maximal hypotensive effect was observed 15 and 10 min after injection, respectively, but the effect was greater and longer‐lasting in the SHR. 8‐OH‐DPAT significantly decreased heart rate in WKY and, to a lesser extent, in SHR. The iv injection of 1 mg/kg of flesinoxan caused a similar fall in blood pressure and heart rate in SHR and WKY. The iv administration of 1 mg/kg of 5‐methyl‐urapidil or MDL 75,608A caused a fall in blood pressure which was significantly more pronounced in SHR than in WKY. 5‐methyl‐urapidil induced a significant tachycardia in WKY, but had little effect on heart rate in SHR. MDL 75,608A caused a short‐lasting tachycardia in SHR and WKY. In conscious SHR, the intracerebroventricular (icv) injection of 10 μg of 8‐OH‐DPAT or 100 μg of either flesinoxan or MDL 75,608A caused a decrease in blood pressure and heart rate. The icv injection of 100 μg of 5‐methyl‐urapidil caused only a decrease in blood pressure. Chronic pre‐treatment with these compounds, by daily iv injection, did not significantly influence the hypotensive or bradycardic effects in an acute experiment. The involvement of α<hi rend="subscript">1</hi>‐adrenoceptors in the effects of these compounds was studied by administering phenylephrine (1 μg/iv) at 5‐ min intervals before and after the iv injection of the experimental compounds. The injection of phenylephrine reproducibly increased blood pressure by 35–40 mm Hg after saline pre‐treatment, and these responses were not affected by the iv injection of 0.1 mg/kg of either 8‐OH‐DPAT or 1 mg/kg of flesinoxan. In contrast, the phenylephrine‐induced pressor responses were markedly diminished at 5 min after treatment with 1 mg/kg of either 5‐methyl‐urapidil or MDL 75,608A, but slowly recovered thereafter. These results show that the 5‐HT<hi rend="subscript">1A</hi> recptor agonists 8‐OH‐DPAT, flesinoxan, 5‐methyl‐urapidil and MDL 75,608A show antihypertensive properties in conscious SHR after iv or icv injection. However, the mechanism of action of the compounds differs: 8‐OH‐DPAT and flesinoxan may act predominantly as 5‐HT<hi rend="subscript">1A</hi> receptor agonists, where as 5‐methyl‐urapidil and MDL 75,608A also seem to have an effect on peripheral α<hi rend="subscript">1</hi>‐adrenoceptors.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">serotonin</term><term xml:id="k2">5‐HT<hi rend="subscript">1A</hi>‐receptor</term><term xml:id="k3">blood pressure</term><term xml:id="k4">heart rate</term><term xml:id="k5">spontaneously hypertensive rat</term><term xml:id="k6">desensitization</term><term xml:id="k7">α<hi rend="subscript">1</hi>‐adrenoceptor</term></keywords><keywords rend="tocHeading1"><term>Original Article</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/A1844558F0EE050164323A09CA7B0F18556CCAC9/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1472-8206</doi><issn type="print">0767-3981</issn><issn type="electronic">1472-8206</issn><idGroup><id type="product" value="FCP"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="FUNDAMENTAL CLINICAL PHARMACOLOGY">Fundamental & Clinical Pharmacology</title></titleGroup></publicationMeta><publicationMeta level="part" position="12009"><doi origin="wiley">10.1111/fcp.1993.7.issue-9</doi><numberingGroup><numbering type="journalVolume" number="7">7</numbering><numbering type="journalIssue" number="9">9</numbering></numberingGroup><coverDate startDate="1993-12">December 1993</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="3" status="forIssue"><doi origin="wiley">10.1111/j.1472-8206.1993.tb00254.x</doi><idGroup><id type="unit" value="FCP254"></id></idGroup><countGroup><count type="pageTotal" number="13"></count></countGroup><titleGroup><title type="tocHeading1">Original Article</title></titleGroup><copyright>1993 Société Française de Pharmacologie et de Thérapeutique</copyright><eventGroup><event type="firstOnline" date="2009-08-26"></event><event type="publishedOnlineFinalForm" date="2009-08-26"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.5 mode:FullText source:HeaderRef result:HeaderRef" date="2010-04-07"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-12"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="499">499</numbering><numbering type="pageLast" number="511">511</numbering></numberingGroup><linkGroup><link type="toTypesetVersion" href="file:FCP.FCP254.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 29 December 1992; accepted 15 June 1993</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="41"></count><count type="linksCrossRef" number="3"></count></countGroup><titleGroup><title type="main">Differential cardiovascular effects of 8‐hydroxy‐2‐(di‐n‐propylamino) tetralin (8‐OH‐DPAT), flesinoxan, 5‐methyl‐urapidil and MDL 75,608A in conscious spontaneously hypertensive rats</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>S.</givenNames><familyName>Buisson‐Defferier</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>M.</givenNames><familyName>Hibert</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>M.</givenNames><familyNamePrefix>van den</familyNamePrefix><familyName>Buuse</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="FR"><unparsedAffiliation>Marion Merrell Dow Research Institute, Strasbourg Research Center, 16, rue d'Ankara, BP 067, 67046 Strasbourg Cedex, France</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="AU"><unparsedAffiliation>Baker Medical Research Institute, Conunercial Road, PO Box 348, Prahran, Vic 3181, Australia</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">serotonin</keyword><keyword xml:id="k2">5‐HT<sub>1A</sub>‐receptor</keyword><keyword xml:id="k3">blood pressure</keyword><keyword xml:id="k4">heart rate</keyword><keyword xml:id="k5">spontaneously hypertensive rat</keyword><keyword xml:id="k6">desensitization</keyword><keyword xml:id="k7">α<sub>1</sub>‐adrenoceptor</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>Summary—</b> The effects of intravenous (iv) administration of four agonists at central 5‐HT<sub>1A</sub> receptors were investigated and compared. Acute iv injection of 0.1 mg/kg of 8‐OH‐DPAT induced a decrease in blood pressure both in spontaneously hypertensive rats (SHR) and normotensive Wistar‐Kyoto rats (WKY). The maximal hypotensive effect was observed 15 and 10 min after injection, respectively, but the effect was greater and longer‐lasting in the SHR. 8‐OH‐DPAT significantly decreased heart rate in WKY and, to a lesser extent, in SHR. The iv injection of 1 mg/kg of flesinoxan caused a similar fall in blood pressure and heart rate in SHR and WKY. The iv administration of 1 mg/kg of 5‐methyl‐urapidil or MDL 75,608A caused a fall in blood pressure which was significantly more pronounced in SHR than in WKY. 5‐methyl‐urapidil induced a significant tachycardia in WKY, but had little effect on heart rate in SHR. MDL 75,608A caused a short‐lasting tachycardia in SHR and WKY. In conscious SHR, the intracerebroventricular (icv) injection of 10 μg of 8‐OH‐DPAT or 100 μg of either flesinoxan or MDL 75,608A caused a decrease in blood pressure and heart rate. The icv injection of 100 μg of 5‐methyl‐urapidil caused only a decrease in blood pressure. Chronic pre‐treatment with these compounds, by daily iv injection, did not significantly influence the hypotensive or bradycardic effects in an acute experiment. The involvement of α<sub>1</sub>‐adrenoceptors in the effects of these compounds was studied by administering phenylephrine (1 μg/iv) at 5‐ min intervals before and after the iv injection of the experimental compounds. The injection of phenylephrine reproducibly increased blood pressure by 35–40 mm Hg after saline pre‐treatment, and these responses were not affected by the iv injection of 0.1 mg/kg of either 8‐OH‐DPAT or 1 mg/kg of flesinoxan. In contrast, the phenylephrine‐induced pressor responses were markedly diminished at 5 min after treatment with 1 mg/kg of either 5‐methyl‐urapidil or MDL 75,608A, but slowly recovered thereafter. These results show that the 5‐HT<sub>1A</sub> recptor agonists 8‐OH‐DPAT, flesinoxan, 5‐methyl‐urapidil and MDL 75,608A show antihypertensive properties in conscious SHR after iv or icv injection. However, the mechanism of action of the compounds differs: 8‐OH‐DPAT and flesinoxan may act predominantly as 5‐HT<sub>1A</sub> receptor agonists, where as 5‐methyl‐urapidil and MDL 75,608A also seem to have an effect on peripheral α<sub>1</sub>‐adrenoceptors.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Differential cardiovascular effects of 8‐hydroxy‐2‐(di‐n‐propylamino) tetralin (8‐OH‐DPAT), flesinoxan, 5‐methyl‐urapidil and MDL 75,608A in conscious spontaneously hypertensive rats</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Differential cardiovascular effects of 8‐hydroxy‐2‐(di‐n‐propylamino) tetralin (8‐OH‐DPAT), flesinoxan, 5‐methyl‐urapidil and MDL 75,608A in conscious spontaneously hypertensive rats</title></titleInfo><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Buisson‐Defferier</namePart><affiliation>Marion Merrell Dow Research Institute, Strasbourg Research Center, 16, rue d'Ankara, BP 067, 67046 Strasbourg Cedex, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Hibert</namePart><affiliation>Marion Merrell Dow Research Institute, Strasbourg Research Center, 16, rue d'Ankara, BP 067, 67046 Strasbourg Cedex, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">van den Buuse</namePart><affiliation>Baker Medical Research Institute, Conunercial Road, PO Box 348, Prahran, Vic 3181, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1993-12</dateIssued><edition>Received 29 December 1992; accepted 15 June 1993</edition><copyrightDate encoding="w3cdtf">1993</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="references">41</extent><extent unit="linksCrossRef">3</extent></physicalDescription><abstract>Summary— The effects of intravenous (iv) administration of four agonists at central 5‐HT1A receptors were investigated and compared. Acute iv injection of 0.1 mg/kg of 8‐OH‐DPAT induced a decrease in blood pressure both in spontaneously hypertensive rats (SHR) and normotensive Wistar‐Kyoto rats (WKY). The maximal hypotensive effect was observed 15 and 10 min after injection, respectively, but the effect was greater and longer‐lasting in the SHR. 8‐OH‐DPAT significantly decreased heart rate in WKY and, to a lesser extent, in SHR. The iv injection of 1 mg/kg of flesinoxan caused a similar fall in blood pressure and heart rate in SHR and WKY. The iv administration of 1 mg/kg of 5‐methyl‐urapidil or MDL 75,608A caused a fall in blood pressure which was significantly more pronounced in SHR than in WKY. 5‐methyl‐urapidil induced a significant tachycardia in WKY, but had little effect on heart rate in SHR. MDL 75,608A caused a short‐lasting tachycardia in SHR and WKY. In conscious SHR, the intracerebroventricular (icv) injection of 10 μg of 8‐OH‐DPAT or 100 μg of either flesinoxan or MDL 75,608A caused a decrease in blood pressure and heart rate. The icv injection of 100 μg of 5‐methyl‐urapidil caused only a decrease in blood pressure. Chronic pre‐treatment with these compounds, by daily iv injection, did not significantly influence the hypotensive or bradycardic effects in an acute experiment. The involvement of α1‐adrenoceptors in the effects of these compounds was studied by administering phenylephrine (1 μg/iv) at 5‐ min intervals before and after the iv injection of the experimental compounds. The injection of phenylephrine reproducibly increased blood pressure by 35–40 mm Hg after saline pre‐treatment, and these responses were not affected by the iv injection of 0.1 mg/kg of either 8‐OH‐DPAT or 1 mg/kg of flesinoxan. In contrast, the phenylephrine‐induced pressor responses were markedly diminished at 5 min after treatment with 1 mg/kg of either 5‐methyl‐urapidil or MDL 75,608A, but slowly recovered thereafter. These results show that the 5‐HT1A recptor agonists 8‐OH‐DPAT, flesinoxan, 5‐methyl‐urapidil and MDL 75,608A show antihypertensive properties in conscious SHR after iv or icv injection. However, the mechanism of action of the compounds differs: 8‐OH‐DPAT and flesinoxan may act predominantly as 5‐HT1A receptor agonists, where as 5‐methyl‐urapidil and MDL 75,608A also seem to have an effect on peripheral α1‐adrenoceptors.</abstract><subject lang="en"><genre>keywords</genre><topic>serotonin</topic><topic>5‐HT1A‐receptor</topic><topic>blood pressure</topic><topic>heart rate</topic><topic>spontaneously hypertensive rat</topic><topic>desensitization</topic><topic>α1‐adrenoceptor</topic></subject><relatedItem type="host"><titleInfo><title>Fundamental & Clinical Pharmacology</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">0767-3981</identifier><identifier type="eISSN">1472-8206</identifier><identifier type="DOI">10.1111/(ISSN)1472-8206</identifier><identifier type="PublisherID">FCP</identifier><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>7</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>499</start><end>511</end><total>13</total></extent></part></relatedItem><identifier type="istex">A1844558F0EE050164323A09CA7B0F18556CCAC9</identifier><identifier type="ark">ark:/67375/WNG-7LXHFB56-W</identifier><identifier type="DOI">10.1111/j.1472-8206.1993.tb00254.x</identifier><identifier type="ArticleID">FCP254</identifier><accessCondition type="use and reproduction" contentType="copyright">1993 Société Française de Pharmacologie et de Thérapeutique</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/A1844558F0EE050164323A09CA7B0F18556CCAC9/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Asie/explor/AustralieFrV1/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001E58 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 001E58 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Asie
|area= AustralieFrV1
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:A1844558F0EE050164323A09CA7B0F18556CCAC9
|texte= Differential cardiovascular effects of 8‐hydroxy‐2‐(di‐n‐propylamino) tetralin (8‐OH‐DPAT), flesinoxan, 5‐methyl‐urapidil and MDL 75,608A in conscious spontaneously hypertensive rats
}}
| This area was generated with Dilib version V0.6.33. |  |