B2 bradykinin receptor (B2BKR) polymorphism and change in left ventricular mass in response to antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial
OBJECTIVEHypertension is associated with a number of adverse morphologic and functional changes in the cardiovascular system, including left ventricular (LV) hypertrophy. Studies have demonstrated that bradykinin, through the B2 bradykinin receptor (B2BKR), mediates important cardiovascular effects...
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| Veröffentlicht in: | Journal of hypertension 2003-03, Vol.21 (3), p.621-624 |
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| creator | Hallberg, Pär Lind, Lars Michaëlsson, Karl Karlsson, Julia Kurland, Lisa Kahan, Thomas Malmqvist, Karin Öhman, K Peter Nyström, Fredrik Melhus, Håkan |
| description | OBJECTIVEHypertension is associated with a number of adverse morphologic and functional changes in the cardiovascular system, including left ventricular (LV) hypertrophy. Studies have demonstrated that bradykinin, through the B2 bradykinin receptor (B2BKR), mediates important cardiovascular effects that may protect against LV hypertrophy. Recently, a +9/−9 exon 1 polymorphism of the B2BKR was shown to be strongly associated with LV growth response among normotensive males undergoing physical training. We aimed to clarify whether the processes found in exercise-induced LV growth in normotensive people also occur in pathological LV hypertrophy.
DESIGN AND METHODSWe determined the B2BKR genotype of 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, included in a double-blind study to receive treatment for 48 weeks with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan or the β1-adrenoceptor antagonist atenolol.
RESULTSB2BKR +9/+9 genotypes responded poorly in LV mass regression, independent of blood pressure reduction or treatment, as compared to the other genotypes (adjusted mean change in LV mass index = −10.0 ± 4.6 versus −21.6 ± 2.2 g/m, P = 0.03).
CONCLUSIONSOur results suggest an impact of the B2BKR polymorphism on LV mass regression during antihypertensive treatment. |
| doi_str_mv | 10.1097/00004872-200303000-00029 |
| format | Article |
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DESIGN AND METHODSWe determined the B2BKR genotype of 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, included in a double-blind study to receive treatment for 48 weeks with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan or the β1-adrenoceptor antagonist atenolol.
RESULTSB2BKR +9/+9 genotypes responded poorly in LV mass regression, independent of blood pressure reduction or treatment, as compared to the other genotypes (adjusted mean change in LV mass index = −10.0 ± 4.6 versus −21.6 ± 2.2 g/m, P = 0.03).
CONCLUSIONSOur results suggest an impact of the B2BKR polymorphism on LV mass regression during antihypertensive treatment.</description><identifier>ISSN: 0263-6352</identifier><identifier>ISSN: 1473-5598</identifier><identifier>EISSN: 1473-5598</identifier><identifier>DOI: 10.1097/00004872-200303000-00029</identifier><identifier>PMID: 12640257</identifier><identifier>CODEN: JOHYD3</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins, Inc</publisher><subject>Adrenergic beta-Antagonists - therapeutic use ; angiotensin ; Angiotensin II Type 1 Receptor Blockers ; Antihypertensive agents ; Antihypertensive Agents - therapeutic use ; atenolol ; Atenolol - therapeutic use ; Biological and medical sciences ; Biphenyl Compounds - therapeutic use ; bradykinin ; Cardiovascular system ; Double-Blind Method ; Female ; Genotype ; heart ; Humans ; hypertension ; Hypertension - drug therapy ; Hypertension - genetics ; Hypertension - pathology ; Hypertrophy, Left Ventricular - drug therapy ; Hypertrophy, Left Ventricular - genetics ; Hypertrophy, Left Ventricular - pathology ; Irbesartan ; left ventricular hypertrophy ; Male ; Medical sciences ; MEDICIN ; Medicin och hälsovetenskap ; MEDICINE ; Middle Aged ; Organ Size - drug effects ; pharmacogenomics ; Pharmacology. Drug treatments ; polymorphism ; Polymorphism, Genetic ; Receptor, Bradykinin B2 - genetics ; Sweden ; Tetrazoles - therapeutic use</subject><ispartof>Journal of hypertension, 2003-03, Vol.21 (3), p.621-624</ispartof><rights>2003 Lippincott Williams & Wilkins, Inc.</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c4919-5ed73c339cc2ce94035245a4ed868618d5882e446a25e81da7e998d912505c1d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,27928,27929</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14686412$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12640257$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-27067$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-69397$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:1938143$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Hallberg, Pär</creatorcontrib><creatorcontrib>Lind, Lars</creatorcontrib><creatorcontrib>Michaëlsson, Karl</creatorcontrib><creatorcontrib>Karlsson, Julia</creatorcontrib><creatorcontrib>Kurland, Lisa</creatorcontrib><creatorcontrib>Kahan, Thomas</creatorcontrib><creatorcontrib>Malmqvist, Karin</creatorcontrib><creatorcontrib>Öhman, K Peter</creatorcontrib><creatorcontrib>Nyström, Fredrik</creatorcontrib><creatorcontrib>Melhus, Håkan</creatorcontrib><title>B2 bradykinin receptor (B2BKR) polymorphism and change in left ventricular mass in response to antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial</title><title>Journal of hypertension</title><addtitle>J Hypertens</addtitle><description>OBJECTIVEHypertension is associated with a number of adverse morphologic and functional changes in the cardiovascular system, including left ventricular (LV) hypertrophy. Studies have demonstrated that bradykinin, through the B2 bradykinin receptor (B2BKR), mediates important cardiovascular effects that may protect against LV hypertrophy. Recently, a +9/−9 exon 1 polymorphism of the B2BKR was shown to be strongly associated with LV growth response among normotensive males undergoing physical training. We aimed to clarify whether the processes found in exercise-induced LV growth in normotensive people also occur in pathological LV hypertrophy.
DESIGN AND METHODSWe determined the B2BKR genotype of 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, included in a double-blind study to receive treatment for 48 weeks with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan or the β1-adrenoceptor antagonist atenolol.
RESULTSB2BKR +9/+9 genotypes responded poorly in LV mass regression, independent of blood pressure reduction or treatment, as compared to the other genotypes (adjusted mean change in LV mass index = −10.0 ± 4.6 versus −21.6 ± 2.2 g/m, P = 0.03).
CONCLUSIONSOur results suggest an impact of the B2BKR polymorphism on LV mass regression during antihypertensive treatment.</description><subject>Adrenergic beta-Antagonists - therapeutic use</subject><subject>angiotensin</subject><subject>Angiotensin II Type 1 Receptor Blockers</subject><subject>Antihypertensive agents</subject><subject>Antihypertensive Agents - therapeutic use</subject><subject>atenolol</subject><subject>Atenolol - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Biphenyl Compounds - therapeutic use</subject><subject>bradykinin</subject><subject>Cardiovascular system</subject><subject>Double-Blind Method</subject><subject>Female</subject><subject>Genotype</subject><subject>heart</subject><subject>Humans</subject><subject>hypertension</subject><subject>Hypertension - drug therapy</subject><subject>Hypertension - genetics</subject><subject>Hypertension - pathology</subject><subject>Hypertrophy, Left Ventricular - drug therapy</subject><subject>Hypertrophy, Left Ventricular - genetics</subject><subject>Hypertrophy, Left Ventricular - pathology</subject><subject>Irbesartan</subject><subject>left ventricular hypertrophy</subject><subject>Male</subject><subject>Medical sciences</subject><subject>MEDICIN</subject><subject>Medicin och hälsovetenskap</subject><subject>MEDICINE</subject><subject>Middle Aged</subject><subject>Organ Size - drug effects</subject><subject>pharmacogenomics</subject><subject>Pharmacology. Drug treatments</subject><subject>polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Receptor, Bradykinin B2 - genetics</subject><subject>Sweden</subject><subject>Tetrazoles - therapeutic use</subject><issn>0263-6352</issn><issn>1473-5598</issn><issn>1473-5598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNk91uFCEYhidGo7V6C4YTTZs4yt_MgGfb-tONm5hY7SlhmW87WGYYgelmL9m7kO1uW0-aCCEQ8rzfS-ClKBDB7wiWzXucGxcNLSnGLHeMyzyofFQcEN6wsqqkeFwcYFqzsmYVfVY8j_FXRoRs2NPiGaE1x7RqDoo_JxQtg243V3awAwpgYEw-oKMTevL1-zEavdv0PoydjT3SQ4tMp4dLQJl1sEroGoYUrJmcDqjXMaKbInH0QwSUfJYk221GCAmGaK_zXgCd-qz6sOUmlyJaBd-j1AE6X0NrY4fmYQlRh6QHtNiaXPxjcnZTLPix26D5cA0x2UudrB_yUUKcIpplJ--8Q0fn88XF2Xx2nD2tdi-KJyvtIrzcz4fFz8-ffpyelYtvX-ans0VpuCSyrKBtmGFMGkMNSI7z9fFKc2hFLWoi2koICpzXmlYgSKsbkFK0ktAKV4a07LAod3XjGsZpqcZgex02ymur9ltXeQWqkrgSLPPNg_wYfHsvuhUSyQThW-XbB5Uf7cVM-XCZx6RqyfK7_xfu7KRog-st_maH50P8nvI9q95GA87pAfwUVcMIrmtGMih2oAk-xgCru8oEq21c1W1c1V1c1U1cs_TV3mNa9tDeC_f5zMDrPaCj0W4V9GBsvOd4fhNOaOb4jlt7l3IOrty0hqA60C516qHvwv4CFRcJGQ</recordid><startdate>200303</startdate><enddate>200303</enddate><creator>Hallberg, Pär</creator><creator>Lind, Lars</creator><creator>Michaëlsson, Karl</creator><creator>Karlsson, Julia</creator><creator>Kurland, Lisa</creator><creator>Kahan, Thomas</creator><creator>Malmqvist, Karin</creator><creator>Öhman, K Peter</creator><creator>Nyström, Fredrik</creator><creator>Melhus, Håkan</creator><general>Lippincott Williams & Wilkins, Inc</general><general>Lippincott Williams & Wilkins</general><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>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>DG8</scope><scope>D91</scope></search><sort><creationdate>200303</creationdate><title>B2 bradykinin receptor (B2BKR) polymorphism and change in left ventricular mass in response to antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial</title><author>Hallberg, Pär ; Lind, Lars ; Michaëlsson, Karl ; Karlsson, Julia ; Kurland, Lisa ; Kahan, Thomas ; Malmqvist, Karin ; Öhman, K Peter ; Nyström, Fredrik ; Melhus, Håkan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4919-5ed73c339cc2ce94035245a4ed868618d5882e446a25e81da7e998d912505c1d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adrenergic beta-Antagonists - therapeutic use</topic><topic>angiotensin</topic><topic>Angiotensin II Type 1 Receptor Blockers</topic><topic>Antihypertensive agents</topic><topic>Antihypertensive Agents - therapeutic use</topic><topic>atenolol</topic><topic>Atenolol - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Biphenyl Compounds - therapeutic use</topic><topic>bradykinin</topic><topic>Cardiovascular system</topic><topic>Double-Blind Method</topic><topic>Female</topic><topic>Genotype</topic><topic>heart</topic><topic>Humans</topic><topic>hypertension</topic><topic>Hypertension - drug therapy</topic><topic>Hypertension - genetics</topic><topic>Hypertension - pathology</topic><topic>Hypertrophy, Left Ventricular - drug therapy</topic><topic>Hypertrophy, Left Ventricular - genetics</topic><topic>Hypertrophy, Left Ventricular - pathology</topic><topic>Irbesartan</topic><topic>left ventricular hypertrophy</topic><topic>Male</topic><topic>Medical sciences</topic><topic>MEDICIN</topic><topic>Medicin och hälsovetenskap</topic><topic>MEDICINE</topic><topic>Middle Aged</topic><topic>Organ Size - drug effects</topic><topic>pharmacogenomics</topic><topic>Pharmacology. Drug treatments</topic><topic>polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Receptor, Bradykinin B2 - genetics</topic><topic>Sweden</topic><topic>Tetrazoles - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hallberg, Pär</creatorcontrib><creatorcontrib>Lind, Lars</creatorcontrib><creatorcontrib>Michaëlsson, Karl</creatorcontrib><creatorcontrib>Karlsson, Julia</creatorcontrib><creatorcontrib>Kurland, Lisa</creatorcontrib><creatorcontrib>Kahan, Thomas</creatorcontrib><creatorcontrib>Malmqvist, Karin</creatorcontrib><creatorcontrib>Öhman, K Peter</creatorcontrib><creatorcontrib>Nyström, Fredrik</creatorcontrib><creatorcontrib>Melhus, Håkan</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>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Linköpings universitet</collection><collection>SWEPUB Örebro universitet</collection><jtitle>Journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hallberg, Pär</au><au>Lind, Lars</au><au>Michaëlsson, Karl</au><au>Karlsson, Julia</au><au>Kurland, Lisa</au><au>Kahan, Thomas</au><au>Malmqvist, Karin</au><au>Öhman, K Peter</au><au>Nyström, Fredrik</au><au>Melhus, Håkan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>B2 bradykinin receptor (B2BKR) polymorphism and change in left ventricular mass in response to antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial</atitle><jtitle>Journal of hypertension</jtitle><addtitle>J Hypertens</addtitle><date>2003-03</date><risdate>2003</risdate><volume>21</volume><issue>3</issue><spage>621</spage><epage>624</epage><pages>621-624</pages><issn>0263-6352</issn><issn>1473-5598</issn><eissn>1473-5598</eissn><coden>JOHYD3</coden><abstract>OBJECTIVEHypertension is associated with a number of adverse morphologic and functional changes in the cardiovascular system, including left ventricular (LV) hypertrophy. Studies have demonstrated that bradykinin, through the B2 bradykinin receptor (B2BKR), mediates important cardiovascular effects that may protect against LV hypertrophy. Recently, a +9/−9 exon 1 polymorphism of the B2BKR was shown to be strongly associated with LV growth response among normotensive males undergoing physical training. We aimed to clarify whether the processes found in exercise-induced LV growth in normotensive people also occur in pathological LV hypertrophy.
DESIGN AND METHODSWe determined the B2BKR genotype of 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, included in a double-blind study to receive treatment for 48 weeks with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan or the β1-adrenoceptor antagonist atenolol.
RESULTSB2BKR +9/+9 genotypes responded poorly in LV mass regression, independent of blood pressure reduction or treatment, as compared to the other genotypes (adjusted mean change in LV mass index = −10.0 ± 4.6 versus −21.6 ± 2.2 g/m, P = 0.03).
CONCLUSIONSOur results suggest an impact of the B2BKR polymorphism on LV mass regression during antihypertensive treatment.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>12640257</pmid><doi>10.1097/00004872-200303000-00029</doi><tpages>4</tpages></addata></record> |
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| subjects | Adrenergic beta-Antagonists - therapeutic use angiotensin Angiotensin II Type 1 Receptor Blockers Antihypertensive agents Antihypertensive Agents - therapeutic use atenolol Atenolol - therapeutic use Biological and medical sciences Biphenyl Compounds - therapeutic use bradykinin Cardiovascular system Double-Blind Method Female Genotype heart Humans hypertension Hypertension - drug therapy Hypertension - genetics Hypertension - pathology Hypertrophy, Left Ventricular - drug therapy Hypertrophy, Left Ventricular - genetics Hypertrophy, Left Ventricular - pathology Irbesartan left ventricular hypertrophy Male Medical sciences MEDICIN Medicin och hälsovetenskap MEDICINE Middle Aged Organ Size - drug effects pharmacogenomics Pharmacology. Drug treatments polymorphism Polymorphism, Genetic Receptor, Bradykinin B2 - genetics Sweden Tetrazoles - therapeutic use |
| title | B2 bradykinin receptor (B2BKR) polymorphism and change in left ventricular mass in response to antihypertensive treatment: results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial |
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