Smoking-dependent effects of the angiotensin-converting enzyme gene insertion/deletion polymorphism on blood pressure
BACKGROUNDStudies on the role of the angiotensin-converting enzyme (ACE) gene in the development of hypertension have yielded conflicting results. Recent studies suggested that this gene might have smoking-dependent effects on the development of cardiovascular disease. OBJECTIVETo study the relation...
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| Veröffentlicht in: | Journal of hypertension 2004-02, Vol.22 (2), p.313-319 |
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| container_title | Journal of hypertension |
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| creator | Schut, Anna FC Sayed-Tabatabaei, Fakhredin A Witteman, Jacqueline CM Avella, Aida MBertoli Vergeer, Jeannette M Pols, Huibert AP Hofman, Albert Deinum, Jaap van Duijn, Cornelia M |
| description | BACKGROUNDStudies on the role of the angiotensin-converting enzyme (ACE) gene in the development of hypertension have yielded conflicting results. Recent studies suggested that this gene might have smoking-dependent effects on the development of cardiovascular disease.
OBJECTIVETo study the relationship between the ACE insertion/deletion (I/D) polymorphism, blood pressure and risk of hypertension in current, former and non-smokers in a population-based cohort.
METHODSWe included 2412 non-smokers, 2794 former smokers and 1508 current smokers, all participants in the Rotterdam Study. In each group, we assessed the relationship between the ACE I/D polymorphism, systolic (SBP) and diastolic (DBP) blood pressures and risk of hypertension. Mean blood pressures and prevalence of hypertension were compared between carriers and non-carriers of the D allele. All analyses were adjusted for age, sex, body mass index, diabetes mellitus, high-density lipoprotein cholesterol, total cholesterol and use of antihypertensive medication.
RESULTSIn non-smokers and former smokers, blood pressure and the risk of hypertension did not differ significantly between genotypes. In smokers, we found a significant increase in SBP in DD carriers (139.6 ± 22.8 mmHg) compared with II carriers (136.0 ± 22.7 mmHg) (P = 0.04). No effect of ACE genotype was observed for DBP. The risk of hypertension was significantly increased in smokers who carried one [odds ratio (OR) 1.4, 95% confidence interval (CI) 1.0 to 1.9; P = 0.05] or two (OR 1.5, 95% CI 1.1 to 2.2; P = 0.02) copies of the D allele.
CONCLUSIONSThe D allele of the ACE polymorphism is associated with a significantly increased SBP and risk of hypertension in smokers. Our study underlines the importance of gene–environment interactions in the study of candidate genes for hypertension. |
| doi_str_mv | 10.1097/00004872-200402000-00015 |
| format | Article |
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OBJECTIVETo study the relationship between the ACE insertion/deletion (I/D) polymorphism, blood pressure and risk of hypertension in current, former and non-smokers in a population-based cohort.
METHODSWe included 2412 non-smokers, 2794 former smokers and 1508 current smokers, all participants in the Rotterdam Study. In each group, we assessed the relationship between the ACE I/D polymorphism, systolic (SBP) and diastolic (DBP) blood pressures and risk of hypertension. Mean blood pressures and prevalence of hypertension were compared between carriers and non-carriers of the D allele. All analyses were adjusted for age, sex, body mass index, diabetes mellitus, high-density lipoprotein cholesterol, total cholesterol and use of antihypertensive medication.
RESULTSIn non-smokers and former smokers, blood pressure and the risk of hypertension did not differ significantly between genotypes. In smokers, we found a significant increase in SBP in DD carriers (139.6 ± 22.8 mmHg) compared with II carriers (136.0 ± 22.7 mmHg) (P = 0.04). No effect of ACE genotype was observed for DBP. The risk of hypertension was significantly increased in smokers who carried one [odds ratio (OR) 1.4, 95% confidence interval (CI) 1.0 to 1.9; P = 0.05] or two (OR 1.5, 95% CI 1.1 to 2.2; P = 0.02) copies of the D allele.
CONCLUSIONSThe D allele of the ACE polymorphism is associated with a significantly increased SBP and risk of hypertension in smokers. Our study underlines the importance of gene–environment interactions in the study of candidate genes for hypertension.</description><identifier>ISSN: 0263-6352</identifier><identifier>EISSN: 1473-5598</identifier><identifier>DOI: 10.1097/00004872-200402000-00015</identifier><identifier>PMID: 15076189</identifier><language>eng</language><publisher>England: Lippincott Williams & Wilkins, Inc</publisher><subject>Aged ; Aged, 80 and over ; Blood Pressure - genetics ; DNA Transposable Elements ; Female ; Gene Deletion ; Genetic Predisposition to Disease ; Genotype ; Heterozygote ; Humans ; Hypertension - etiology ; Hypertension - genetics ; Male ; Middle Aged ; Peptidyl-Dipeptidase A - genetics ; Polymorphism, Genetic ; Smoking - adverse effects ; Systole</subject><ispartof>Journal of hypertension, 2004-02, Vol.22 (2), p.313-319</ispartof><rights>2004 Lippincott Williams & Wilkins, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3565-10fc9ef0c8dee3568c8640d2d5674e5a49e4b095c73221bf7981d563952b35263</citedby><cites>FETCH-LOGICAL-c3565-10fc9ef0c8dee3568c8640d2d5674e5a49e4b095c73221bf7981d563952b35263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15076189$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schut, Anna FC</creatorcontrib><creatorcontrib>Sayed-Tabatabaei, Fakhredin A</creatorcontrib><creatorcontrib>Witteman, Jacqueline CM</creatorcontrib><creatorcontrib>Avella, Aida MBertoli</creatorcontrib><creatorcontrib>Vergeer, Jeannette M</creatorcontrib><creatorcontrib>Pols, Huibert AP</creatorcontrib><creatorcontrib>Hofman, Albert</creatorcontrib><creatorcontrib>Deinum, Jaap</creatorcontrib><creatorcontrib>van Duijn, Cornelia M</creatorcontrib><title>Smoking-dependent effects of the angiotensin-converting enzyme gene insertion/deletion polymorphism on blood pressure</title><title>Journal of hypertension</title><addtitle>J Hypertens</addtitle><description>BACKGROUNDStudies on the role of the angiotensin-converting enzyme (ACE) gene in the development of hypertension have yielded conflicting results. Recent studies suggested that this gene might have smoking-dependent effects on the development of cardiovascular disease.
OBJECTIVETo study the relationship between the ACE insertion/deletion (I/D) polymorphism, blood pressure and risk of hypertension in current, former and non-smokers in a population-based cohort.
METHODSWe included 2412 non-smokers, 2794 former smokers and 1508 current smokers, all participants in the Rotterdam Study. In each group, we assessed the relationship between the ACE I/D polymorphism, systolic (SBP) and diastolic (DBP) blood pressures and risk of hypertension. Mean blood pressures and prevalence of hypertension were compared between carriers and non-carriers of the D allele. All analyses were adjusted for age, sex, body mass index, diabetes mellitus, high-density lipoprotein cholesterol, total cholesterol and use of antihypertensive medication.
RESULTSIn non-smokers and former smokers, blood pressure and the risk of hypertension did not differ significantly between genotypes. In smokers, we found a significant increase in SBP in DD carriers (139.6 ± 22.8 mmHg) compared with II carriers (136.0 ± 22.7 mmHg) (P = 0.04). No effect of ACE genotype was observed for DBP. The risk of hypertension was significantly increased in smokers who carried one [odds ratio (OR) 1.4, 95% confidence interval (CI) 1.0 to 1.9; P = 0.05] or two (OR 1.5, 95% CI 1.1 to 2.2; P = 0.02) copies of the D allele.
CONCLUSIONSThe D allele of the ACE polymorphism is associated with a significantly increased SBP and risk of hypertension in smokers. Our study underlines the importance of gene–environment interactions in the study of candidate genes for hypertension.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Blood Pressure - genetics</subject><subject>DNA Transposable Elements</subject><subject>Female</subject><subject>Gene Deletion</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Heterozygote</subject><subject>Humans</subject><subject>Hypertension - etiology</subject><subject>Hypertension - genetics</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Peptidyl-Dipeptidase A - genetics</subject><subject>Polymorphism, Genetic</subject><subject>Smoking - adverse effects</subject><subject>Systole</subject><issn>0263-6352</issn><issn>1473-5598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc9PHCEUgElTU1fbf8Fw8kblxzDA0ZhWTUw8VM9khnmzO8rACDM1279etru2J0ngweN7ED4Qwox-Z9SoC1papRUnvERaBkpKZ_ITWrFKCSKl0Z_RivJakFpIfoxOcn4qiDZKfEHHTFJVM21WaPk1xuchrEkHE4QOwoyh78HNGccezxvATVgPcYaQh0BcDL8hzYXHEP5sR8BrCICHkHfZGC468LCb4Cn67RjTtBnyiMu69TF2eEqQ85LgKzrqG5_h2yGeosefPx6ubsjd_fXt1eUdcULWkjDaOwM9dboDKBntdF3RjneyVhXIpjJQtdRIpwTnrO2V0azsCSN5W15di1N0vj93SvFlgTzbccgOvG8CxCVbxTSvK0ELqPegSzHnBL2d0jA2aWsZtTvl9l25_afc_lVeSs8OdyztCN3_woPjAlR74DX6GVJ-9ssrJLuBxs8b-9FXijetEo3n</recordid><startdate>200402</startdate><enddate>200402</enddate><creator>Schut, Anna FC</creator><creator>Sayed-Tabatabaei, Fakhredin A</creator><creator>Witteman, Jacqueline CM</creator><creator>Avella, Aida MBertoli</creator><creator>Vergeer, Jeannette M</creator><creator>Pols, Huibert AP</creator><creator>Hofman, Albert</creator><creator>Deinum, Jaap</creator><creator>van Duijn, Cornelia M</creator><general>Lippincott Williams & Wilkins, Inc</general><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></search><sort><creationdate>200402</creationdate><title>Smoking-dependent effects of the angiotensin-converting enzyme gene insertion/deletion polymorphism on blood pressure</title><author>Schut, Anna FC ; Sayed-Tabatabaei, Fakhredin A ; Witteman, Jacqueline CM ; Avella, Aida MBertoli ; Vergeer, Jeannette M ; Pols, Huibert AP ; Hofman, Albert ; Deinum, Jaap ; van Duijn, Cornelia M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3565-10fc9ef0c8dee3568c8640d2d5674e5a49e4b095c73221bf7981d563952b35263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Blood Pressure - genetics</topic><topic>DNA Transposable Elements</topic><topic>Female</topic><topic>Gene Deletion</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Heterozygote</topic><topic>Humans</topic><topic>Hypertension - etiology</topic><topic>Hypertension - genetics</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Peptidyl-Dipeptidase A - genetics</topic><topic>Polymorphism, Genetic</topic><topic>Smoking - adverse effects</topic><topic>Systole</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schut, Anna FC</creatorcontrib><creatorcontrib>Sayed-Tabatabaei, Fakhredin A</creatorcontrib><creatorcontrib>Witteman, Jacqueline CM</creatorcontrib><creatorcontrib>Avella, Aida MBertoli</creatorcontrib><creatorcontrib>Vergeer, Jeannette M</creatorcontrib><creatorcontrib>Pols, Huibert AP</creatorcontrib><creatorcontrib>Hofman, Albert</creatorcontrib><creatorcontrib>Deinum, Jaap</creatorcontrib><creatorcontrib>van Duijn, Cornelia M</creatorcontrib><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><jtitle>Journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schut, Anna FC</au><au>Sayed-Tabatabaei, Fakhredin A</au><au>Witteman, Jacqueline CM</au><au>Avella, Aida MBertoli</au><au>Vergeer, Jeannette M</au><au>Pols, Huibert AP</au><au>Hofman, Albert</au><au>Deinum, Jaap</au><au>van Duijn, Cornelia M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Smoking-dependent effects of the angiotensin-converting enzyme gene insertion/deletion polymorphism on blood pressure</atitle><jtitle>Journal of hypertension</jtitle><addtitle>J Hypertens</addtitle><date>2004-02</date><risdate>2004</risdate><volume>22</volume><issue>2</issue><spage>313</spage><epage>319</epage><pages>313-319</pages><issn>0263-6352</issn><eissn>1473-5598</eissn><abstract>BACKGROUNDStudies on the role of the angiotensin-converting enzyme (ACE) gene in the development of hypertension have yielded conflicting results. Recent studies suggested that this gene might have smoking-dependent effects on the development of cardiovascular disease.
OBJECTIVETo study the relationship between the ACE insertion/deletion (I/D) polymorphism, blood pressure and risk of hypertension in current, former and non-smokers in a population-based cohort.
METHODSWe included 2412 non-smokers, 2794 former smokers and 1508 current smokers, all participants in the Rotterdam Study. In each group, we assessed the relationship between the ACE I/D polymorphism, systolic (SBP) and diastolic (DBP) blood pressures and risk of hypertension. Mean blood pressures and prevalence of hypertension were compared between carriers and non-carriers of the D allele. All analyses were adjusted for age, sex, body mass index, diabetes mellitus, high-density lipoprotein cholesterol, total cholesterol and use of antihypertensive medication.
RESULTSIn non-smokers and former smokers, blood pressure and the risk of hypertension did not differ significantly between genotypes. In smokers, we found a significant increase in SBP in DD carriers (139.6 ± 22.8 mmHg) compared with II carriers (136.0 ± 22.7 mmHg) (P = 0.04). No effect of ACE genotype was observed for DBP. The risk of hypertension was significantly increased in smokers who carried one [odds ratio (OR) 1.4, 95% confidence interval (CI) 1.0 to 1.9; P = 0.05] or two (OR 1.5, 95% CI 1.1 to 2.2; P = 0.02) copies of the D allele.
CONCLUSIONSThe D allele of the ACE polymorphism is associated with a significantly increased SBP and risk of hypertension in smokers. Our study underlines the importance of gene–environment interactions in the study of candidate genes for hypertension.</abstract><cop>England</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>15076189</pmid><doi>10.1097/00004872-200402000-00015</doi><tpages>7</tpages></addata></record> |
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| ispartof | Journal of hypertension, 2004-02, Vol.22 (2), p.313-319 |
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| source | MEDLINE; Journals@Ovid Complete |
| subjects | Aged Aged, 80 and over Blood Pressure - genetics DNA Transposable Elements Female Gene Deletion Genetic Predisposition to Disease Genotype Heterozygote Humans Hypertension - etiology Hypertension - genetics Male Middle Aged Peptidyl-Dipeptidase A - genetics Polymorphism, Genetic Smoking - adverse effects Systole |
| title | Smoking-dependent effects of the angiotensin-converting enzyme gene insertion/deletion polymorphism on blood pressure |
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