The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein
The mechanisms underlying the suppression of vasocontractility caused by progesterone were investigated by studying changes in the contractile force of rat isolated aorta and portal vein, induced by altering extracellular concentrations of noradrenaline (NA) potassium ions (K+) and calcium ions (Ca2...
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| Veröffentlicht in: | Journal of pharmacy and pharmacology 2000-07, Vol.52 (7), p.843-849 |
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| container_title | Journal of pharmacy and pharmacology |
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| creator | MUKERJI, MARK S. LEATHARD, HELEN L. HUDDART, HENRY |
| description | The mechanisms underlying the suppression of vasocontractility caused by progesterone were investigated by studying changes in the contractile force of rat isolated aorta and portal vein, induced by altering extracellular concentrations of noradrenaline (NA) potassium ions (K+) and calcium ions (Ca2+).
In the aorta, progesterone (10 μM) had a general suppressive effect on NA‐, Ca2+‐ and K+‐induced contractions. In contrast, in the portal vein a more selective suppression of contractions was observed. Both tonic and phasic components of contractions induced by cumulative addition of Ca2+ to tissues equilibrated in Ca2+‐free saline were suppressed. The phasic but not tonic components of contractions induced by NA addition were suppressed. There was no significant effect on tonic contractions induced by elevated (40–120 mM) K+, but a concentration‐dependent suppression of the phasic component of contractions was observed during depolarisation with smaller elevations of K+ concentrations (5–20 mM).
These results suggest that on the portal vein the suppressive effect of progesterone is due to a potassium channel opening action, whilst on the aorta a different or additional mechanism of suppression exists. |
| doi_str_mv | 10.1211/0022357001774525 |
| format | Article |
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In the aorta, progesterone (10 μM) had a general suppressive effect on NA‐, Ca2+‐ and K+‐induced contractions. In contrast, in the portal vein a more selective suppression of contractions was observed. Both tonic and phasic components of contractions induced by cumulative addition of Ca2+ to tissues equilibrated in Ca2+‐free saline were suppressed. The phasic but not tonic components of contractions induced by NA addition were suppressed. There was no significant effect on tonic contractions induced by elevated (40–120 mM) K+, but a concentration‐dependent suppression of the phasic component of contractions was observed during depolarisation with smaller elevations of K+ concentrations (5–20 mM).
These results suggest that on the portal vein the suppressive effect of progesterone is due to a potassium channel opening action, whilst on the aorta a different or additional mechanism of suppression exists.</description><identifier>ISSN: 0022-3573</identifier><identifier>EISSN: 2042-7158</identifier><identifier>DOI: 10.1211/0022357001774525</identifier><identifier>PMID: 10933135</identifier><identifier>CODEN: JPPMAB</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Aorta - drug effects ; Biological and medical sciences ; Calcium - pharmacology ; Cardiovascular system ; Drug Interactions ; In Vitro Techniques ; Male ; Medical sciences ; Miscellaneous ; Norepinephrine - pharmacology ; Pharmacology. Drug treatments ; Portal Vein - drug effects ; Potassium - pharmacology ; Progesterone - pharmacology ; Rats ; Rats, Wistar ; Vasoconstriction - drug effects ; Vasoconstrictor Agents - pharmacology</subject><ispartof>Journal of pharmacy and pharmacology, 2000-07, Vol.52 (7), p.843-849</ispartof><rights>2000 Royal Pharmaceutical Society of Great Britain</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4819-e5f574e6a289f20c6341b07bfbadc7dc1e1da802b567ae2d860d0d843a8a26fd3</citedby><cites>FETCH-LOGICAL-c4819-e5f574e6a289f20c6341b07bfbadc7dc1e1da802b567ae2d860d0d843a8a26fd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1211%2F0022357001774525$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1211%2F0022357001774525$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,27923,27924,45573,45574</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1402860$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10933135$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MUKERJI, MARK S.</creatorcontrib><creatorcontrib>LEATHARD, HELEN L.</creatorcontrib><creatorcontrib>HUDDART, HENRY</creatorcontrib><title>The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein</title><title>Journal of pharmacy and pharmacology</title><addtitle>J Pharm Pharmacol</addtitle><description>The mechanisms underlying the suppression of vasocontractility caused by progesterone were investigated by studying changes in the contractile force of rat isolated aorta and portal vein, induced by altering extracellular concentrations of noradrenaline (NA) potassium ions (K+) and calcium ions (Ca2+).
In the aorta, progesterone (10 μM) had a general suppressive effect on NA‐, Ca2+‐ and K+‐induced contractions. In contrast, in the portal vein a more selective suppression of contractions was observed. Both tonic and phasic components of contractions induced by cumulative addition of Ca2+ to tissues equilibrated in Ca2+‐free saline were suppressed. The phasic but not tonic components of contractions induced by NA addition were suppressed. There was no significant effect on tonic contractions induced by elevated (40–120 mM) K+, but a concentration‐dependent suppression of the phasic component of contractions was observed during depolarisation with smaller elevations of K+ concentrations (5–20 mM).
These results suggest that on the portal vein the suppressive effect of progesterone is due to a potassium channel opening action, whilst on the aorta a different or additional mechanism of suppression exists.</description><subject>Animals</subject><subject>Aorta - drug effects</subject><subject>Biological and medical sciences</subject><subject>Calcium - pharmacology</subject><subject>Cardiovascular system</subject><subject>Drug Interactions</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Miscellaneous</subject><subject>Norepinephrine - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Portal Vein - drug effects</subject><subject>Potassium - pharmacology</subject><subject>Progesterone - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Vasoconstriction - drug effects</subject><subject>Vasoconstrictor Agents - pharmacology</subject><issn>0022-3573</issn><issn>2042-7158</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhi1ERZfCnRPyAXFLGduxnRxXq6VLW5WIFpC4WI4_StpsvLWz0P77eskKEBdOtjTPM555jdArAseEEvIOgFLGJQCRsuSUP0EzCiUtJOHVUzTblYtcZ4foeUo3ACCFEM_QIYGaMcL4DN1cfXd46b0zIw4eNzFcuzS6GAaHw4AvN2EY9eDCNmE9WDy_DkOXxmL5I9w6ixe5GrUZuzCknT7mZp_0iOchjvqX0OxuPf7iuuEFOvC6T-7l_jxCn98vrxar4vzjyYfF_LwwZUXqwnHPZemEplXtKRjBStKCbH2rrZHWEEesroC2XEjtqK0EWLBVyXSlqfCWHaG3U99NDHfbvI1ad8m4vp_2UBQEITXIDMIEmhhSis6rTezWOj4oAmqXr_o336y83vfetmtn_xKmQDPwZg_oZHTvox5Ml_5wJdA8cMb4hP3sevfw33fVabNqJKmzV0xe_gR3_9vT8VYJySRXXy9OFFs0p5erb2eKs0emsqBM</recordid><startdate>200007</startdate><enddate>200007</enddate><creator>MUKERJI, MARK S.</creator><creator>LEATHARD, HELEN L.</creator><creator>HUDDART, HENRY</creator><general>Blackwell Publishing Ltd</general><general>Pharmaceutical Press</general><scope>BSCLL</scope><scope>IQODW</scope><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>7QP</scope></search><sort><creationdate>200007</creationdate><title>The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein</title><author>MUKERJI, MARK S. ; LEATHARD, HELEN L. ; HUDDART, HENRY</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4819-e5f574e6a289f20c6341b07bfbadc7dc1e1da802b567ae2d860d0d843a8a26fd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Aorta - drug effects</topic><topic>Biological and medical sciences</topic><topic>Calcium - pharmacology</topic><topic>Cardiovascular system</topic><topic>Drug Interactions</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Miscellaneous</topic><topic>Norepinephrine - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Portal Vein - drug effects</topic><topic>Potassium - pharmacology</topic><topic>Progesterone - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Vasoconstriction - drug effects</topic><topic>Vasoconstrictor Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MUKERJI, MARK S.</creatorcontrib><creatorcontrib>LEATHARD, HELEN L.</creatorcontrib><creatorcontrib>HUDDART, HENRY</creatorcontrib><collection>Istex</collection><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>Calcium & Calcified Tissue Abstracts</collection><jtitle>Journal of pharmacy and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MUKERJI, MARK S.</au><au>LEATHARD, HELEN L.</au><au>HUDDART, HENRY</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein</atitle><jtitle>Journal of pharmacy and pharmacology</jtitle><addtitle>J Pharm Pharmacol</addtitle><date>2000-07</date><risdate>2000</risdate><volume>52</volume><issue>7</issue><spage>843</spage><epage>849</epage><pages>843-849</pages><issn>0022-3573</issn><eissn>2042-7158</eissn><coden>JPPMAB</coden><abstract>The mechanisms underlying the suppression of vasocontractility caused by progesterone were investigated by studying changes in the contractile force of rat isolated aorta and portal vein, induced by altering extracellular concentrations of noradrenaline (NA) potassium ions (K+) and calcium ions (Ca2+).
In the aorta, progesterone (10 μM) had a general suppressive effect on NA‐, Ca2+‐ and K+‐induced contractions. In contrast, in the portal vein a more selective suppression of contractions was observed. Both tonic and phasic components of contractions induced by cumulative addition of Ca2+ to tissues equilibrated in Ca2+‐free saline were suppressed. The phasic but not tonic components of contractions induced by NA addition were suppressed. There was no significant effect on tonic contractions induced by elevated (40–120 mM) K+, but a concentration‐dependent suppression of the phasic component of contractions was observed during depolarisation with smaller elevations of K+ concentrations (5–20 mM).
These results suggest that on the portal vein the suppressive effect of progesterone is due to a potassium channel opening action, whilst on the aorta a different or additional mechanism of suppression exists.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>10933135</pmid><doi>10.1211/0022357001774525</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of pharmacy and pharmacology, 2000-07, Vol.52 (7), p.843-849 |
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| source | MEDLINE; Oxford University Press Journals All Titles (1996-Current); Wiley Online Library All Journals |
| subjects | Animals Aorta - drug effects Biological and medical sciences Calcium - pharmacology Cardiovascular system Drug Interactions In Vitro Techniques Male Medical sciences Miscellaneous Norepinephrine - pharmacology Pharmacology. Drug treatments Portal Vein - drug effects Potassium - pharmacology Progesterone - pharmacology Rats Rats, Wistar Vasoconstriction - drug effects Vasoconstrictor Agents - pharmacology |
| title | The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein |
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