Enhanced blood pressure sensitivity to DOCA‐salt treatment in endothelin ETB receptor‐deficient rats
The role of endothelin ETB receptor‐mediated action in the development and maintenance of deoxycorticosterone acetate (DOCA)‐salt‐induced hypertension was evaluated using the spotting‐lethal (sl) rat which carries a naturally occurring deletion in the ETB receptor gene. Homozygous (sl/sl) rats treat...
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description | The role of endothelin ETB receptor‐mediated action in the development and maintenance of deoxycorticosterone acetate (DOCA)‐salt‐induced hypertension was evaluated using the spotting‐lethal (sl) rat which carries a naturally occurring deletion in the ETB receptor gene. Homozygous (sl/sl) rats treated with DOCA‐salt for 1 week exhibited an earlier onset of hypertension than heterozygous (sl/+) and wild‐type (+/+) rats (systolic blood pressure, SBP; 156.7±3.4 versus 128.8±5.3 and 132.9±3.7 mmHg, respectively). Four weeks after the start of DOCA‐salt treatment, homozygous rats developed marked hypertension, with a SBP of 206.0±4.5 mmHg, compared with 184.8±10.7 mmHg in heterozygous and 164.3±4.8 mmHg in wild‐type rats. Cardiovascular hypertrophy and renal dysfunction observed after 4‐weeks treatment with DOCA‐salt were more severe in homozygous rats, compared to wild‐type and heterozygous animals. These evidences support strongly the view that ETB receptor‐mediated actions are a protective factor in the pathogenesis of DOCA‐salt‐induced hypertension.
British Journal of Pharmacology (2000) 129, 1060–1062; doi:10.1038/sj.bjp.0703157 |
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British Journal of Pharmacology (2000) 129, 1060–1062; doi:10.1038/sj.bjp.0703157</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0703157</identifier><identifier>PMID: 10725252</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Biological and medical sciences ; deoxycorticosterone acetate‐salt hypertension ; endothelin‐1 ; ETB receptor ; Medical sciences ; Neuropharmacology ; Neurotransmitters. Neurotransmission. Receptors ; Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems ; Pharmacology. Drug treatments ; renal function ; Special Reports</subject><ispartof>British journal of pharmacology, 2000-03, Vol.129 (6), p.1060-1062</ispartof><rights>2000 British Pharmacological Society</rights><rights>2000 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Mar 2000</rights><rights>Copyright 2000, Nature Publishing Group 2000 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/PMC1571939/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1571939/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1297387$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>Matsumura, Yasuo</creatorcontrib><creatorcontrib>Kuro, Toshihiko</creatorcontrib><creatorcontrib>Konishi, Fumiko</creatorcontrib><creatorcontrib>Takaoka, Masanori</creatorcontrib><creatorcontrib>Gariepy, Cheryl E</creatorcontrib><creatorcontrib>Yanagisawa, Masashi</creatorcontrib><title>Enhanced blood pressure sensitivity to DOCA‐salt treatment in endothelin ETB receptor‐deficient rats</title><title>British journal of pharmacology</title><description>The role of endothelin ETB receptor‐mediated action in the development and maintenance of deoxycorticosterone acetate (DOCA)‐salt‐induced hypertension was evaluated using the spotting‐lethal (sl) rat which carries a naturally occurring deletion in the ETB receptor gene. Homozygous (sl/sl) rats treated with DOCA‐salt for 1 week exhibited an earlier onset of hypertension than heterozygous (sl/+) and wild‐type (+/+) rats (systolic blood pressure, SBP; 156.7±3.4 versus 128.8±5.3 and 132.9±3.7 mmHg, respectively). Four weeks after the start of DOCA‐salt treatment, homozygous rats developed marked hypertension, with a SBP of 206.0±4.5 mmHg, compared with 184.8±10.7 mmHg in heterozygous and 164.3±4.8 mmHg in wild‐type rats. Cardiovascular hypertrophy and renal dysfunction observed after 4‐weeks treatment with DOCA‐salt were more severe in homozygous rats, compared to wild‐type and heterozygous animals. These evidences support strongly the view that ETB receptor‐mediated actions are a protective factor in the pathogenesis of DOCA‐salt‐induced hypertension.
British Journal of Pharmacology (2000) 129, 1060–1062; doi:10.1038/sj.bjp.0703157</description><subject>Biological and medical sciences</subject><subject>deoxycorticosterone acetate‐salt hypertension</subject><subject>endothelin‐1</subject><subject>ETB receptor</subject><subject>Medical sciences</subject><subject>Neuropharmacology</subject><subject>Neurotransmitters. Neurotransmission. Receptors</subject><subject>Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems</subject><subject>Pharmacology. Drug treatments</subject><subject>renal function</subject><subject>Special Reports</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNpVkcFqGzEURUVoSBy3265F6daunuQZSZtC4rpJIJAu0rXQjN7UGsajqSSneNdP6DfmS6oQ0xK0kNA93Pe4l5D3wJbAhPqU-mXTT0smmYBKnpAZrGS9qISCN2TGGJMLAKXOyUVKPWNFlNUZOQcmeVXOjGw349aOLTraDCE4OkVMaR-RJhyTz_7R5wPNgX65X18-_f6T7JBpjmjzDsdM_UhxdCFvcSjPzcMVjdjilEMsrMPOt_4Zizant-S0s0PCd8d7Tr5_3TysbxZ399e368u7xcRV2VYB50wx3ulWMwt1hzXyZlU-QNpGrxTU0GjurGuURMcdyJWuQVlZt7aSrZiTzy--077ZoWvL_GgHM0W_s_FggvXmtTL6rfkRHk2JD7TQxeDD0SCGn3tM2fRhH8eys-EgQWpRgp-Tj0fIptYOXSwZ-vRvCnAthZIFEy_YLz_g4b_MzHN5JvWmlGeO5ZmrbzeiFlL8BZP2kXo</recordid><startdate>200003</startdate><enddate>200003</enddate><creator>Matsumura, Yasuo</creator><creator>Kuro, Toshihiko</creator><creator>Konishi, Fumiko</creator><creator>Takaoka, Masanori</creator><creator>Gariepy, Cheryl E</creator><creator>Yanagisawa, Masashi</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><scope>IQODW</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>200003</creationdate><title>Enhanced blood pressure sensitivity to DOCA‐salt treatment in endothelin ETB receptor‐deficient rats</title><author>Matsumura, Yasuo ; Kuro, Toshihiko ; Konishi, Fumiko ; Takaoka, Masanori ; Gariepy, Cheryl E ; Yanagisawa, Masashi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p2807-81220802f9c90a16fe6e2b402f17ab948161b92dadb87ed2d1749618a76ca57c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Biological and medical sciences</topic><topic>deoxycorticosterone acetate‐salt hypertension</topic><topic>endothelin‐1</topic><topic>ETB receptor</topic><topic>Medical sciences</topic><topic>Neuropharmacology</topic><topic>Neurotransmitters. Neurotransmission. Receptors</topic><topic>Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems</topic><topic>Pharmacology. Drug treatments</topic><topic>renal function</topic><topic>Special Reports</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matsumura, Yasuo</creatorcontrib><creatorcontrib>Kuro, Toshihiko</creatorcontrib><creatorcontrib>Konishi, Fumiko</creatorcontrib><creatorcontrib>Takaoka, Masanori</creatorcontrib><creatorcontrib>Gariepy, Cheryl E</creatorcontrib><creatorcontrib>Yanagisawa, Masashi</creatorcontrib><collection>Pascal-Francis</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</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>Matsumura, Yasuo</au><au>Kuro, Toshihiko</au><au>Konishi, Fumiko</au><au>Takaoka, Masanori</au><au>Gariepy, Cheryl E</au><au>Yanagisawa, Masashi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhanced blood pressure sensitivity to DOCA‐salt treatment in endothelin ETB receptor‐deficient rats</atitle><jtitle>British journal of pharmacology</jtitle><date>2000-03</date><risdate>2000</risdate><volume>129</volume><issue>6</issue><spage>1060</spage><epage>1062</epage><pages>1060-1062</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>The role of endothelin ETB receptor‐mediated action in the development and maintenance of deoxycorticosterone acetate (DOCA)‐salt‐induced hypertension was evaluated using the spotting‐lethal (sl) rat which carries a naturally occurring deletion in the ETB receptor gene. Homozygous (sl/sl) rats treated with DOCA‐salt for 1 week exhibited an earlier onset of hypertension than heterozygous (sl/+) and wild‐type (+/+) rats (systolic blood pressure, SBP; 156.7±3.4 versus 128.8±5.3 and 132.9±3.7 mmHg, respectively). Four weeks after the start of DOCA‐salt treatment, homozygous rats developed marked hypertension, with a SBP of 206.0±4.5 mmHg, compared with 184.8±10.7 mmHg in heterozygous and 164.3±4.8 mmHg in wild‐type rats. Cardiovascular hypertrophy and renal dysfunction observed after 4‐weeks treatment with DOCA‐salt were more severe in homozygous rats, compared to wild‐type and heterozygous animals. These evidences support strongly the view that ETB receptor‐mediated actions are a protective factor in the pathogenesis of DOCA‐salt‐induced hypertension.
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subjects | Biological and medical sciences deoxycorticosterone acetate‐salt hypertension endothelin‐1 ETB receptor Medical sciences Neuropharmacology Neurotransmitters. Neurotransmission. Receptors Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems Pharmacology. Drug treatments renal function Special Reports |
title | Enhanced blood pressure sensitivity to DOCA‐salt treatment in endothelin ETB receptor‐deficient rats |
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