Mechanisms Mediating the Vasoactive Effects of the B1 Receptors of Bradykinin
ABSTRACT—Bradykinin normally exerts its vasodilatory effect via the B2 receptor (B2R), but in this receptor’s absence, the B1 receptor becomes expressed and activated. To explore the mechanism of B1R-mediated vasodilation, 8 groups of B2R gene–knockout mice received a 2-week infusion of a B1R antago...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2003-11, Vol.42 (5), p.1021-1025 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Duka, Irena Duka, Arvi Kintsurashvili, Ekaterina Johns, Conrado Gavras, Irene Gavras, Haralambos |
| description | ABSTRACT—Bradykinin normally exerts its vasodilatory effect via the B2 receptor (B2R), but in this receptor’s absence, the B1 receptor becomes expressed and activated. To explore the mechanism of B1R-mediated vasodilation, 8 groups of B2R gene–knockout mice received a 2-week infusion of a B1R antagonist (300 μg · kg · d) or vehicle (groups 1 and 2), B1R antagonist or vehicle plus NO inhibition with Nω-nitro-l-arginine methyl ester (groups 3 and 4), B1R antagonist or vehicle plus cyclooxygenase inhibition with indomethacin (groups 5 and 6), or B1R antagonist or vehicle plus blockade of vasoconstricting prostaglandin (PG) H2 and thromboxane A2 (TxA2) with SQ29548 (groups 7 and 8). The B1R antagonist produced significant (P |
| doi_str_mv | 10.1161/01.HYP.0000097550.98865.35 |
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To explore the mechanism of B1R-mediated vasodilation, 8 groups of B2R gene–knockout mice received a 2-week infusion of a B1R antagonist (300 μg · kg · d) or vehicle (groups 1 and 2), B1R antagonist or vehicle plus NO inhibition with Nω-nitro-l-arginine methyl ester (groups 3 and 4), B1R antagonist or vehicle plus cyclooxygenase inhibition with indomethacin (groups 5 and 6), or B1R antagonist or vehicle plus blockade of vasoconstricting prostaglandin (PG) H2 and thromboxane A2 (TxA2) with SQ29548 (groups 7 and 8). The B1R antagonist produced significant (P <0.05) blood pressure increases of 17.7±3.1 mm Hg in group 1 and 10.4±3 mm Hg in group 3, whereas their vehicle-treated respective control groups 2 and 4 had no significant blood pressure changes. Indomethacin abolished the capacity of the B1R antagonist to raise blood pressure, as did blockade of the receptors of PGH2 and TxA2. Injection with the B1R agonist produced a hypotensive response (12±1.3 mm Hg), which was further accentuated by TxA2 blockade (21.7±4.1 mm Hg). Analysis of B1R gene expression by reverse transcription–polymerase chain reaction (PCR) in cardiac and renal tissues revealed marked expression at baseline, with further upregulation by 1.5- to 2-fold after various manipulations. Expression of the TxA2 receptor gene in renal tissue by quantitative real-time PCR was significantly lower in mice treated with the B1R antagonist, consistent with increased levels of agonist for this receptor. The data confirm that the B1R becomes markedly expressed in the absence of B2R and suggest that it contributes to vasodilation by inhibiting a vasoconstricting product of the arachidonic acid cascade acting via the PGH2/TxA2 receptor.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.HYP.0000097550.98865.35</identifier><identifier>PMID: 14557281</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Animals ; Biological and medical sciences ; Blood Pressure - drug effects ; Blood vessels and receptors ; Bradykinin B1 Receptor Antagonists ; Cyclooxygenase Inhibitors - pharmacology ; Enzyme Inhibitors - pharmacology ; Fundamental and applied biological sciences. Psychology ; Hydrazines - pharmacology ; Indomethacin - pharmacology ; Mice ; Mice, Knockout ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric Oxide Synthase - antagonists & inhibitors ; Receptor, Bradykinin B1 - genetics ; Receptor, Bradykinin B1 - physiology ; Receptor, Bradykinin B2 - genetics ; Receptor, Bradykinin B2 - physiology ; Receptors, Thromboxane A2, Prostaglandin H2 - antagonists & inhibitors ; RNA, Messenger - metabolism ; Vasodilation ; Vertebrates: cardiovascular system</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2003-11, Vol.42 (5), p.1021-1025</ispartof><rights>2003 American Heart Association, Inc.</rights><rights>2004 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Nov 2003</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15267031$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14557281$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Duka, Irena</creatorcontrib><creatorcontrib>Duka, Arvi</creatorcontrib><creatorcontrib>Kintsurashvili, Ekaterina</creatorcontrib><creatorcontrib>Johns, Conrado</creatorcontrib><creatorcontrib>Gavras, Irene</creatorcontrib><creatorcontrib>Gavras, Haralambos</creatorcontrib><title>Mechanisms Mediating the Vasoactive Effects of the B1 Receptors of Bradykinin</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>ABSTRACT—Bradykinin normally exerts its vasodilatory effect via the B2 receptor (B2R), but in this receptor’s absence, the B1 receptor becomes expressed and activated. To explore the mechanism of B1R-mediated vasodilation, 8 groups of B2R gene–knockout mice received a 2-week infusion of a B1R antagonist (300 μg · kg · d) or vehicle (groups 1 and 2), B1R antagonist or vehicle plus NO inhibition with Nω-nitro-l-arginine methyl ester (groups 3 and 4), B1R antagonist or vehicle plus cyclooxygenase inhibition with indomethacin (groups 5 and 6), or B1R antagonist or vehicle plus blockade of vasoconstricting prostaglandin (PG) H2 and thromboxane A2 (TxA2) with SQ29548 (groups 7 and 8). The B1R antagonist produced significant (P <0.05) blood pressure increases of 17.7±3.1 mm Hg in group 1 and 10.4±3 mm Hg in group 3, whereas their vehicle-treated respective control groups 2 and 4 had no significant blood pressure changes. Indomethacin abolished the capacity of the B1R antagonist to raise blood pressure, as did blockade of the receptors of PGH2 and TxA2. Injection with the B1R agonist produced a hypotensive response (12±1.3 mm Hg), which was further accentuated by TxA2 blockade (21.7±4.1 mm Hg). Analysis of B1R gene expression by reverse transcription–polymerase chain reaction (PCR) in cardiac and renal tissues revealed marked expression at baseline, with further upregulation by 1.5- to 2-fold after various manipulations. Expression of the TxA2 receptor gene in renal tissue by quantitative real-time PCR was significantly lower in mice treated with the B1R antagonist, consistent with increased levels of agonist for this receptor. The data confirm that the B1R becomes markedly expressed in the absence of B2R and suggest that it contributes to vasodilation by inhibiting a vasoconstricting product of the arachidonic acid cascade acting via the PGH2/TxA2 receptor.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Blood vessels and receptors</subject><subject>Bradykinin B1 Receptor Antagonists</subject><subject>Cyclooxygenase Inhibitors - pharmacology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hydrazines - pharmacology</subject><subject>Indomethacin - pharmacology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Receptor, Bradykinin B1 - genetics</subject><subject>Receptor, Bradykinin B1 - physiology</subject><subject>Receptor, Bradykinin B2 - genetics</subject><subject>Receptor, Bradykinin B2 - physiology</subject><subject>Receptors, Thromboxane A2, Prostaglandin H2 - antagonists & inhibitors</subject><subject>RNA, Messenger - metabolism</subject><subject>Vasodilation</subject><subject>Vertebrates: cardiovascular system</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpd0V9rFDEQAPAgir2efgVZCvq2ayb_82hLbYUeiqjo05JmJ27avd0z2bX025trTwTzkknmR5iZEHICtAFQ8JZCc_njU0P3y2opaWONUbLh8glZgWSiFlLxp2RFwYraAnw_Isc531AKQgj9nByBkFIzAyuy2aDv3RjzNlcb7KKb4_izmnusvrk8OT_H31idh4B-ztUUHjKnUH1Gj7t5Sg93p8l197dxjOML8iy4IePLw74mX9-ffzm7rK8-Xnw4e3dV90wpqEu1BhV6Kw2TInDBOGi87oQTOgTAYDqNVnZdadBZZa3D0mnQ3jgqmKV8Td48vrtL068F89xuY_Y4DG7EacmtBi6M4azAk__gzbSksdTWMiqZobJMak1eHdByvcWu3aW4dem-_TulAl4fgMveDSG50cf8z0mmNOV7Jx7d3TTMmPLtsNxhant0w9y3--8STJma0YKhnGq6j_gfb-uF2Q</recordid><startdate>200311</startdate><enddate>200311</enddate><creator>Duka, Irena</creator><creator>Duka, Arvi</creator><creator>Kintsurashvili, Ekaterina</creator><creator>Johns, Conrado</creator><creator>Gavras, Irene</creator><creator>Gavras, Haralambos</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>200311</creationdate><title>Mechanisms Mediating the Vasoactive Effects of the B1 Receptors of Bradykinin</title><author>Duka, Irena ; Duka, Arvi ; Kintsurashvili, Ekaterina ; Johns, Conrado ; Gavras, Irene ; Gavras, Haralambos</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h2661-8868e6ec958254f342317ebd4a47ff1ef8d7e95dd000a9699ae009f7c8a042903</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Blood vessels and receptors</topic><topic>Bradykinin B1 Receptor Antagonists</topic><topic>Cyclooxygenase Inhibitors - pharmacology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hydrazines - pharmacology</topic><topic>Indomethacin - pharmacology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Receptor, Bradykinin B1 - genetics</topic><topic>Receptor, Bradykinin B1 - physiology</topic><topic>Receptor, Bradykinin B2 - genetics</topic><topic>Receptor, Bradykinin B2 - physiology</topic><topic>Receptors, Thromboxane A2, Prostaglandin H2 - antagonists & inhibitors</topic><topic>RNA, Messenger - metabolism</topic><topic>Vasodilation</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Duka, Irena</creatorcontrib><creatorcontrib>Duka, Arvi</creatorcontrib><creatorcontrib>Kintsurashvili, Ekaterina</creatorcontrib><creatorcontrib>Johns, Conrado</creatorcontrib><creatorcontrib>Gavras, Irene</creatorcontrib><creatorcontrib>Gavras, Haralambos</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Duka, Irena</au><au>Duka, Arvi</au><au>Kintsurashvili, Ekaterina</au><au>Johns, Conrado</au><au>Gavras, Irene</au><au>Gavras, Haralambos</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms Mediating the Vasoactive Effects of the B1 Receptors of Bradykinin</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2003-11</date><risdate>2003</risdate><volume>42</volume><issue>5</issue><spage>1021</spage><epage>1025</epage><pages>1021-1025</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>ABSTRACT—Bradykinin normally exerts its vasodilatory effect via the B2 receptor (B2R), but in this receptor’s absence, the B1 receptor becomes expressed and activated. To explore the mechanism of B1R-mediated vasodilation, 8 groups of B2R gene–knockout mice received a 2-week infusion of a B1R antagonist (300 μg · kg · d) or vehicle (groups 1 and 2), B1R antagonist or vehicle plus NO inhibition with Nω-nitro-l-arginine methyl ester (groups 3 and 4), B1R antagonist or vehicle plus cyclooxygenase inhibition with indomethacin (groups 5 and 6), or B1R antagonist or vehicle plus blockade of vasoconstricting prostaglandin (PG) H2 and thromboxane A2 (TxA2) with SQ29548 (groups 7 and 8). The B1R antagonist produced significant (P <0.05) blood pressure increases of 17.7±3.1 mm Hg in group 1 and 10.4±3 mm Hg in group 3, whereas their vehicle-treated respective control groups 2 and 4 had no significant blood pressure changes. Indomethacin abolished the capacity of the B1R antagonist to raise blood pressure, as did blockade of the receptors of PGH2 and TxA2. Injection with the B1R agonist produced a hypotensive response (12±1.3 mm Hg), which was further accentuated by TxA2 blockade (21.7±4.1 mm Hg). Analysis of B1R gene expression by reverse transcription–polymerase chain reaction (PCR) in cardiac and renal tissues revealed marked expression at baseline, with further upregulation by 1.5- to 2-fold after various manipulations. Expression of the TxA2 receptor gene in renal tissue by quantitative real-time PCR was significantly lower in mice treated with the B1R antagonist, consistent with increased levels of agonist for this receptor. The data confirm that the B1R becomes markedly expressed in the absence of B2R and suggest that it contributes to vasodilation by inhibiting a vasoconstricting product of the arachidonic acid cascade acting via the PGH2/TxA2 receptor.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>14557281</pmid><doi>10.1161/01.HYP.0000097550.98865.35</doi><tpages>5</tpages></addata></record> |
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| identifier | ISSN: 0194-911X |
| ispartof | Hypertension (Dallas, Tex. 1979), 2003-11, Vol.42 (5), p.1021-1025 |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Biological and medical sciences Blood Pressure - drug effects Blood vessels and receptors Bradykinin B1 Receptor Antagonists Cyclooxygenase Inhibitors - pharmacology Enzyme Inhibitors - pharmacology Fundamental and applied biological sciences. Psychology Hydrazines - pharmacology Indomethacin - pharmacology Mice Mice, Knockout NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide Synthase - antagonists & inhibitors Receptor, Bradykinin B1 - genetics Receptor, Bradykinin B1 - physiology Receptor, Bradykinin B2 - genetics Receptor, Bradykinin B2 - physiology Receptors, Thromboxane A2, Prostaglandin H2 - antagonists & inhibitors RNA, Messenger - metabolism Vasodilation Vertebrates: cardiovascular system |
| title | Mechanisms Mediating the Vasoactive Effects of the B1 Receptors of Bradykinin |
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