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  • 1.
    Alehagen, Urban
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Kardiologiska kliniken US.
    Vorkapic, Emina
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Medicinska fakulteten.
    Ljungberg, Liza
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Medicinska fakulteten.
    Länne, Toste
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Thorax-kärlkliniken i Östergötland.
    Wågsäter, Dick
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för läkemedelsforskning. Linköpings universitet, Medicinska fakulteten.
    Gender difference in adiponectin associated with cardiovascular mortality2015Inngår i: BMC Medical Genetics, ISSN 1471-2350, E-ISSN 1471-2350, Vol. 16, nr 9Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: It is important to identify cardiovascular diseases in patients at high risk. To include genetics into routine cardiological patients has therefore been discussed recently. We wanted to evaluate the association between high-molecular weight adiponectin and cardiovascular risk, and secondly in the same population evaluate if specific genotype differences regarding risk could be observed, and thirdly if gender differences could be seen. Method: Four hundred seventy-six elderly participants recruited from a rural community were included. All participants underwent a clinical examination, echocardiography, and blood sampling and the single nucleotide polymorphism (SNP) (rs266729) of adiponectin was analysed. Follow-up time was 6.7 years. Results: Those with high serum concentration of adiponectin had a more 2 fold increased cardiovascular risk, and it might be that females exhibits even higher risk where a more than 5 fold increased risk could be seen. The result could be demonstrated even in a multivariate model adjusting for well-known clinical risk factors. However, as the sample size was small the gender differences should be interpreted with caution. In the genotype evaluation the C/C carriers of the female group had a more than 9-fold increased risk of cardiovascular mortality, however the confidence interval was wide. Such genotype difference could not be found in the male group. Conclusion: High level of adiponectin was associated with increased cardiovascular risk. Also a gender difference in the genotype evaluation could be seen where the C/C carriers obtained higher risk in the female group but not in the male group. Thus, in order to identify patients at risk early, genetic analyses may add to the armamentarium used in the clinical routine. However, information should be regarded as hypothesis generating as the sample size was small and should stimulate further research in individualized cardiovascular prevention and treatment.

  • 2.
    Björck, Hanna
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet.
    Eriksson, Per
    Karolinska Institute, Stockholm.
    Alehagen, Urban
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Kardiologiska kliniken US.
    Debasso, Rachel
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet.
    Ljungberg, Liza
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Persson, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Dahlström, Ulf
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Kardiologiska kliniken US.
    Länne, Toste
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Thorax-kärlkliniken i Östergötland.
    Gender-Specific Association of the Plasminogen Activator Inhibitor-1 4G/5G Polymorphism With Central Arterial Blood Pressure2011Inngår i: American Journal of Hypertension, ISSN 0895-7061, E-ISSN 1941-7225, Vol. 24, nr 7, s. 802-808Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND The functional plasminogen activator inhibitor-1 (PAI-1) 4G/5G polymorphism has previously been associated with hypertension. In recent years, central blood pressure, rather than brachial has been argued a better measure of cardiovascular damage and clinical outcome. The aim of this study was to investigate the possible influence of the 4G/5G polymorphism on central arterial blood pressure in a cohort of elderly individuals. METHODS We studied 410 individuals, 216 men and 194 women, aged 70-88. Central pressures and pulse waveforms were calculated from the radial artery pressure waveform by the use of the SphygmoCor system and a generalized transfer function. Brachial pressure was recorded using oscillometric technique (Dinamap, Critikon, Tampa, FL). PAI-1 antigen was determined in plasma. RESULTS The results showed that central pressures were higher in women carrying the PAI-1 4G/4G genotype compared to female carriers of the 5G/5G genotype, (P = 0.025, P = 0.002, and P = 0.002 for central systolic-, diastolic-, and mean arterial pressure, respectively). The association remained after adjustment for potentially confounding factors related to hypertension. No association of the PAI-1 genotype with blood pressure was found in men. Multiple regression analysis revealed an association between PAI-1 genotype and plasma PAI-1 levels (P = 0.048). CONCLUSIONS Our findings show a gender-specific association of the PAI-1 4G/5G polymorphism with central arterial blood pressure. The genotype effect was independent of other risk factors related to hypertension, suggesting that impaired fibrinolytic potential may play an important role in the development of central hypertension in women.

  • 3. Bestill onlineKjøp publikasjonen >>
    Ljungberg, Liza
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Angiotensin-Converting Enzyme: Effects of Smoking and Other Risk Factors for Cardiovascular Diseases2009Licentiatavhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    Cardiovascular diseases (CVDs) are the most common cause of death in Western countries. Smoking, hypertension, diabetes mellitus and hypercholesterolemia are considered as major risk factors. However, the underlying mechanisms by which these factors cause CVDs are not entirely clear. Angiotensin-converting enzyme (ACE) is a key enzyme in the renin-angiotensin-aldosterone system, converting angiotensin I to the vasoactive peptide angiotensin II. Besides being an important factor for normal regulation of blood pressure, ACE appears to be involved in the pathogenesis of atherosclerosis. Previous studies have shown an upregulation of ACE in atherosclerotic plaques. There is genetic polymorphism in the ACE gene (ACE I/D polymorphism) which is strongly connected to the levels of ACE in plasma, but has also been associated with higher risk for cardiovascular diseases. The aim of this thesis was to investigate ACE in vitro and in vivo, in relation to cardiovascular risk factors and CVDs. The results showed that nicotine and nicotine metabolites increase ACE activity in human endothelial cells in vitro. Smoking was associated with increased plasma ACE levels. This effect might be mediated by nicotine and nicotine metabolites. These results could explain one cellular mechanism by which smoking exerts negative effect on the vascular system. Extract of oral snuff inhibited ACE in human endothelial cells and in serum, whereas extract of cigarette smoke had no effect on endothelial ACE. If these results have any physiological relevance remains to be investigated. Cardiovascular risk factors and CVDs were associated with increased levels of ACE in plasma. No association between ACE D/D genotype and CVDs was found. Based on these results we suggest that an increased level of ACE, rather than ACE genotype, is associated with increased risk for CVDs.

    Delarbeid
    1. Effect of Nicotine and Nicotine Metabolites on Angiotensin-Converting Enzyme in Human Endothelial Cells
    Åpne denne publikasjonen i ny fane eller vindu >>Effect of Nicotine and Nicotine Metabolites on Angiotensin-Converting Enzyme in Human Endothelial Cells
    2008 (engelsk)Inngår i: Endothelium, ISSN 1062-3329, E-ISSN 1029-2373, Vol. 15, nr 5-6, s. 239-245Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Nicotine has been shown to induce endothelial dysfunction, which is an early marker of atherosclerosis. Nicotine undergoes extensive metabolism in the liver, forming a number of major and minor metabolites. There are very limited data on the effect of nicotine metabolites on the cardiovascular system. This study investigates the effects of nicotine and the nicotine metabolites, cotinine, cotinine-N-oxide, nicotine-1-N-oxide, norcotinine, trans-3-hydroxycotinine, on angiotensin-converting enzyme (ACE) in human endothelial cells. Cultured endothelial cells obtained from human umbilical cord vein (HUVECs) were stimulated with nicotine or nicotine metabolites in concentrations similar to those observed in plasma during smoking. ACE activity and expression were analyzed using commercial kits. The results showed that nicotine and nicotine metabolites can increase both activity and expression of ACE. However, a marked individual variation in the response to the drugs was observed. This variation was not associated with the ACE insertion/deletion polymorphism. Tobacco contains numerous chemical compounds, and the underlying cause for development of atherosclerosis in smokers is probably multifactorial. The results from this study could explain one cellular mechanism by which smoking exerts negative effect on the vascular system.

    Emneord
    Angiotensin-Converting Enzyme, Atherosclerosis, Endothelial Cells, Nicotine, Nicotine Metabolites, Tobacco
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-16216 (URN)10.1080/10623320802487627 (DOI)
    Merknad
    This is an electronic version of an article published in:Liza Ljungberg and Karin Persson, Effect of Nicotine and Nicotine Metabolites on Angiotensin-Converting Enzyme in Human Endothelial Cells, 2008, Endothelium, (15), 5-6, 239-245.Endothelium is available online at informaworldTM: http://dx.doi.org/10.1080/10623320802487627Copyright: Taylor & Francishttp://www.tandf.co.uk/journals/default.aspTilgjengelig fra: 2009-04-08 Laget: 2009-01-09 Sist oppdatert: 2017-12-14bibliografisk kontrollert
    2. Is ACE level rather than ACE genotype a risk factor for cardiovascular disease?
    Åpne denne publikasjonen i ny fane eller vindu >>Is ACE level rather than ACE genotype a risk factor for cardiovascular disease?
    Vise andre…
    (engelsk)Manuskript (Annet vitenskapelig)
    Abstract [en]

    Background: Polymorphism in the angiotensin-converting enzyme gene (ACE I/D polymorphism) is associated with the level of ACE in plasma. However, there are large variations in plasma ACE level among individuals with the same genotype. Furthermore, ACE D/D genotype has been associated with increased risk for cardiovascular disease. The aim of this study was to investigate variations in plasma ACE levels in order to elucidate the associations between circulating ACE levels, ACE genotype, known cardiovascular risk factors and cardiovascular diseases (CVDs).

    Methods and Results: Plasma ACE levels and ACE genotype were analysed in a Swedish population consisting of 672 elderly men and women. Association between ACE-genotype, levels of circulating ACE and known cardiovascular risk factors and CVDs were analyzed. The results showed increased plasma ACE levels in individuals with hypertension (p=0.003), ischemic heart disease (p=0.03), in smokers (p=0.011) and in individuals with heredity for CVDs (p=0.031). Furthermore, treatment with ACE inhibitors increased the level of ACE in plasma (p<0.001). No association was found between D/D genotype and CVD. Instead, ischemic heart disease was more frequent among carriers of the I/I genotype (p=0.009).

    Conclusion: Although plasma ACE levels are strongly influenced by ACE genotype, there are large variations in plasma ACE level among carriers of the same genotype. Our data does not support an association between ACE D/D polymorphism and CVDs but indicates an association to increased level of ACE in the circulation, suggesting that ACE level rather than ACE genotype is the crucial factor associated with risk for CVDs.

    Emneord
    Atherosclerosis, endothelium, genetics, hypertension, smoking
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-16703 (URN)
    Tilgjengelig fra: 2009-02-12 Laget: 2009-02-12 Sist oppdatert: 2017-03-27bibliografisk kontrollert
  • 4. Bestill onlineKjøp publikasjonen >>
    Ljungberg, Liza
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet.
    Angiotensin-converting enzyme in cardiovascular function and dysfunction2011Doktoravhandling, med artikler (Annet vitenskapelig)
    Abstract [en]

    Angiotensin-converting enzyme (ACE) is a key enzyme in the renin-angiotensin system, converting angiotensin I to the vasoactive peptide angiotensin II, and degrading bradykinin. Angiotensin II is a multifunctional peptide, acting on a number of different tissues. A common genetic variation in the gene encoding ACE; ACE I/D polymorphism influences the level of ACE in the circulation, and has been linked to increased risk for cardiovascular disease. This thesis aimed to explore the connection between ACE and cardiovascular function and dysfunction.

    The impact of nicotine and nicotine metabolites on ACE in cultured human endothelial cells was studied. Nicotine as well as nicotine metabolites induced increased ACE activity in cultured human endothelial cells. In elderly men a higher ACE level was seen in smokers compared to non-smokers. Furthermore, diabetes was associated with higher circulating ACE. Increased ACE level may represent a cellular mechanism which contributes to vascular damage.

    Elderly men carrying the ACE D allele had higher abdominal aortic stiffness compared to men carrying the I/I genotype. Our data suggest that the mechanism by which the ACE D allele modulates aortic wall mechanics is independent of circulating ACE levels. Previous studies have indicated a link between the D allele and abdominal aortic aneurysm. Increased aortic stiffness suggests impaired vessel wall integrity, which combined with local hemodynamic and/or inflammatory factors may have a role in aneurysm formation.

    Subjects with left ventricular dysfunction had higher levels of circulating ACE compared to those with normal left ventricular function, while there was no association between ACE and central hemodynamics. ACE might play a role in the pathogenesis of left ventricular dysfunction and our findings suggest a direct effect on the heart rather than affecting central blood pressure.

    Delarbeid
    1. Effect of Nicotine and Nicotine Metabolites on Angiotensin-Converting Enzyme in Human Endothelial Cells
    Åpne denne publikasjonen i ny fane eller vindu >>Effect of Nicotine and Nicotine Metabolites on Angiotensin-Converting Enzyme in Human Endothelial Cells
    2008 (engelsk)Inngår i: Endothelium, ISSN 1062-3329, E-ISSN 1029-2373, Vol. 15, nr 5-6, s. 239-245Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Nicotine has been shown to induce endothelial dysfunction, which is an early marker of atherosclerosis. Nicotine undergoes extensive metabolism in the liver, forming a number of major and minor metabolites. There are very limited data on the effect of nicotine metabolites on the cardiovascular system. This study investigates the effects of nicotine and the nicotine metabolites, cotinine, cotinine-N-oxide, nicotine-1-N-oxide, norcotinine, trans-3-hydroxycotinine, on angiotensin-converting enzyme (ACE) in human endothelial cells. Cultured endothelial cells obtained from human umbilical cord vein (HUVECs) were stimulated with nicotine or nicotine metabolites in concentrations similar to those observed in plasma during smoking. ACE activity and expression were analyzed using commercial kits. The results showed that nicotine and nicotine metabolites can increase both activity and expression of ACE. However, a marked individual variation in the response to the drugs was observed. This variation was not associated with the ACE insertion/deletion polymorphism. Tobacco contains numerous chemical compounds, and the underlying cause for development of atherosclerosis in smokers is probably multifactorial. The results from this study could explain one cellular mechanism by which smoking exerts negative effect on the vascular system.

    Emneord
    Angiotensin-Converting Enzyme, Atherosclerosis, Endothelial Cells, Nicotine, Nicotine Metabolites, Tobacco
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-16216 (URN)10.1080/10623320802487627 (DOI)
    Merknad
    This is an electronic version of an article published in:Liza Ljungberg and Karin Persson, Effect of Nicotine and Nicotine Metabolites on Angiotensin-Converting Enzyme in Human Endothelial Cells, 2008, Endothelium, (15), 5-6, 239-245.Endothelium is available online at informaworldTM: http://dx.doi.org/10.1080/10623320802487627Copyright: Taylor & Francishttp://www.tandf.co.uk/journals/default.aspTilgjengelig fra: 2009-04-08 Laget: 2009-01-09 Sist oppdatert: 2017-12-14bibliografisk kontrollert
    2. The association between circulating angiotensin-converting enzyme and cardiovascular risk in the elderly: A cross-sectional study.
    Åpne denne publikasjonen i ny fane eller vindu >>The association between circulating angiotensin-converting enzyme and cardiovascular risk in the elderly: A cross-sectional study.
    Vise andre…
    2011 (engelsk)Inngår i: jraas. Journal of the renin-angiotensin-aldosterone system, ISSN 1470-3203, E-ISSN 1752-8976, Vol. 12, nr 3, s. 281-289Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    INTRODUCTION: A polymorphism in the angiotensin-converting enzyme gene (ACE I/D polymorphism) has been associated with increased risk for cardiovascular disease (CVD). This polymorphism affects the level of circulating ACE, but there is great individual variation, even between those with the same genotype. Few previous studies have investigated the link between circulating ACE and cardiovascular risk. The aim of this study was to investigate this association, and to examine the relationship between ACE level, ACE genotype and CVD.

    MATERIALS AND METHODS: The study population consisted of 322 men and 350 women aged 69-87. Plasma ACE level was determined using enzyme-linked immunosorbent assay (ELISA), and ACE genotype was analysed using PCR followed by gel electrophoresis.

    RESULTS: In men, ACE levels increased with increasing number of cardiovascular risk factors (p = 0.003). There was a significant association in men between increased ACE level and both diabetes (p = 0.007) and smoking (p = 0.037).

    CONCLUSIONS: This study shows that cardiovascular risk factors (such as smoking and diabetes) are associated with higher levels of circulating ACE in men. High ACE levels may represent one of the cellular mechanisms involved in producing the vascular damage associated with cardiovascular risk factors.

    sted, utgiver, år, opplag, sider
    SAGE, 2011
    Emneord
    Cardiovascular risk factors, dibetes, endothelium, genetics, smoking
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-67208 (URN)10.1177/1470320310391326 (DOI)000294450600019 ()21273224 (PubMedID)
    Merknad
    Funding Agencies|Cardiovascular Inflammatory Research Center, Linkoping, Sweden||Swedish Research Council|
    1216
    |Elanora Demeroutis Foundation, Linkoping, Sweden|
    LIO-28471
    |Goljes Memorial Foundation, Sweden|
    LA2009-0119
    |Medical Research Council of South East Sweden|
    FORSS-34931
    |Tilgjengelig fra: 2011-04-04 Laget: 2011-04-04 Sist oppdatert: 2017-12-11bibliografisk kontrollert
    3. Impaired abdominal aortic wall integrity in elderly men carrying the angiotensin-converting enzyme D allele
    Åpne denne publikasjonen i ny fane eller vindu >>Impaired abdominal aortic wall integrity in elderly men carrying the angiotensin-converting enzyme D allele
    Vise andre…
    2011 (engelsk)Inngår i: European Journal of Vascular and Endovascular Surgery, ISSN 1078-5884, E-ISSN 1532-2165, Vol. 42, nr 3, s. 309-316Artikkel i tidsskrift (Fagfellevurdert) Published
    Abstract [en]

    Objective: A genetic polymorphism in the angiotensin-converting enzyme gene (ACE I/D polymorphism) has been associated with abdominal aortic aneurysm and a link between aortic aneurysm and aortic stiffness has been suggested. The aim of this study was to explore the links between ACE I/D polymorphism, circulating ACE, and abdominal aortic wall integrity as reflected by abdominal aortic wall stiffness.

    Material: The study population consisted of 406 subjects (212 men and 194 women) aged 70-88 years.

    Methods: The mechanical properties of the abdominal aorta were determined 3-4 cm proximal to the aortic bifurcation using a Wall Track System. ACE-genotype was determined by PCR followed by gel electrophoresis, and circulating ACE level was measured by ELISA.

    Results: Men carrying the ACE D allele had lower distensibility coefficient than II carriers (ID/DD 8.09 vs II 10.38, P=0.017). Multiple regression analyses showed additional associations between the ACE D allele and increased stiffness β as well as reduced cross-sectional compliance.

    Conclusion: This study showed that men carrying the ACE D allele have stiffer abdominal aortas compared to II carriers. Deranged abdominal aortic stiffness indicates impaired vessel wall integrity, which along with other local predisposing factors, may be of importance in aneurysmal disease.

    sted, utgiver, år, opplag, sider
    Elsevier, 2011
    Emneord
    Aorta; Arterial stiffness; Distensibility; Gene polymorphism; Mechanical properties
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-67213 (URN)10.1016/j.ejvs.2011.04.010 (DOI)000295061800007 ()
    Tilgjengelig fra: 2011-04-04 Laget: 2011-04-04 Sist oppdatert: 2017-12-11bibliografisk kontrollert
    4. Circulating angiotensin-converting enzyme levels are associated with left ventricular dysfunction, but not with central aortic blood pressure, aortic augmentation or pulse pressure amplification
    Åpne denne publikasjonen i ny fane eller vindu >>Circulating angiotensin-converting enzyme levels are associated with left ventricular dysfunction, but not with central aortic blood pressure, aortic augmentation or pulse pressure amplification
    Vise andre…
    2011 (engelsk)Manuskript (preprint) (Annet vitenskapelig)
    Abstract [en]

    Aim: This study aimed to explore the link between angiotensin-converting enzyme (ACE), and left ventricular (LV) function and central hemodynamics.

    Methods and Results: The study population consisted of 672 subjects (322 men and 350 women) aged 69-87 years. LV function was evaluated semi-quantitatively by visual estimation using echocardiography. Central aortic blood pressure, aortic augmentation and pulse pressure amplification were determined in a sub-group of 422 subjects by the use of the SphygmoCor system. ACE genotype was determined by PCR and circulating ACE levels were analysed using enzyme-linked immunosorbent assay (ELISA).

    LV dysfunction was associated with higher levels of circulating ACE compared to subjects with normal LV function (p=0.007). This association remained after adjustment for factors previously shown to affect circulating ACE (ACE-genotype, age, diabetes and smoking) (p=0.036). There was a significant association between ACE level and degree of LV dysfunction (p=0.019). However, there was no association of ACE genotype or circulating ACE with central aortic blood pressure, aortic augmentation or pulse pressure amplification.

    Conclusion: Subjects with LV dysfunction have higher levels of circulating ACE compared to subjects with normal LV function. ACE might play a role in the pathogenesis of LV dysfunction and our data indicates a direct effect on the heart rather than affecting central blood pressure.

    Emneord
    ACE, Heart Failure, Polymorphism, Renin-Angiotensin System, Central hemodynamics
    HSV kategori
    Identifikatorer
    urn:nbn:se:liu:diva-67214 (URN)
    Tilgjengelig fra: 2011-04-04 Laget: 2011-04-04 Sist oppdatert: 2017-03-27bibliografisk kontrollert
  • 5.
    Ljungberg, Liza
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Alehagen, Urban
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Björck, Hanna
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet.
    Länne, Toste
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärtcentrum, Thorax-kärlkliniken.
    Debasso, Rachel
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet.
    Dahlström, Ulf
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Persson, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    IS ACE LEVEL RATHER THAN ACE GENOTYPE A RISK FACTOR FOR CARDIOVASCULAR DISEASE?2009Inngår i: in JOURNAL OF HYPERTENSION, vol 27, 2009, Vol. 27, s. S455-S455Konferansepaper (Fagfellevurdert)
    Abstract [en]

    n/a

  • 6.
    Ljungberg, Liza
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi.
    Alehagen, Urban
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Björck, Hanna
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi.
    Toste, Länne
    Linköpings universitet, Institutionen för medicin och hälsa. Linköpings universitet, Hälsouniversitetet.
    DeBasso, Rachel
    Dahlström, Ulf
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Persson, Karin
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi.
    Is ACE level rather than ACE genotype a risk factor for cardiovascular disease?Manuskript (Annet vitenskapelig)
    Abstract [en]

    Background: Polymorphism in the angiotensin-converting enzyme gene (ACE I/D polymorphism) is associated with the level of ACE in plasma. However, there are large variations in plasma ACE level among individuals with the same genotype. Furthermore, ACE D/D genotype has been associated with increased risk for cardiovascular disease. The aim of this study was to investigate variations in plasma ACE levels in order to elucidate the associations between circulating ACE levels, ACE genotype, known cardiovascular risk factors and cardiovascular diseases (CVDs).

    Methods and Results: Plasma ACE levels and ACE genotype were analysed in a Swedish population consisting of 672 elderly men and women. Association between ACE-genotype, levels of circulating ACE and known cardiovascular risk factors and CVDs were analyzed. The results showed increased plasma ACE levels in individuals with hypertension (p=0.003), ischemic heart disease (p=0.03), in smokers (p=0.011) and in individuals with heredity for CVDs (p=0.031). Furthermore, treatment with ACE inhibitors increased the level of ACE in plasma (p<0.001). No association was found between D/D genotype and CVD. Instead, ischemic heart disease was more frequent among carriers of the I/I genotype (p=0.009).

    Conclusion: Although plasma ACE levels are strongly influenced by ACE genotype, there are large variations in plasma ACE level among carriers of the same genotype. Our data does not support an association between ACE D/D polymorphism and CVDs but indicates an association to increased level of ACE in the circulation, suggesting that ACE level rather than ACE genotype is the crucial factor associated with risk for CVDs.

  • 7.
    Ljungberg, Liza
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Alehagen, Urban
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Kardiologiska kliniken US.
    De Basso, Rachel
    Linköpings universitet, Institutionen för medicin och hälsa. Linköpings universitet, Hälsouniversitetet.
    Persson, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Dahlström, Ulf
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Kardiologiska kliniken US.
    Länne, Toste
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Thorax-kärlkliniken i Östergötland.
    Circulating angiotensin-converting enzyme levels are associated with left ventricular dysfunction, but not with central aortic blood pressure, aortic augmentation or pulse pressure amplification2011Manuskript (preprint) (Annet vitenskapelig)
    Abstract [en]

    Aim: This study aimed to explore the link between angiotensin-converting enzyme (ACE), and left ventricular (LV) function and central hemodynamics.

    Methods and Results: The study population consisted of 672 subjects (322 men and 350 women) aged 69-87 years. LV function was evaluated semi-quantitatively by visual estimation using echocardiography. Central aortic blood pressure, aortic augmentation and pulse pressure amplification were determined in a sub-group of 422 subjects by the use of the SphygmoCor system. ACE genotype was determined by PCR and circulating ACE levels were analysed using enzyme-linked immunosorbent assay (ELISA).

    LV dysfunction was associated with higher levels of circulating ACE compared to subjects with normal LV function (p=0.007). This association remained after adjustment for factors previously shown to affect circulating ACE (ACE-genotype, age, diabetes and smoking) (p=0.036). There was a significant association between ACE level and degree of LV dysfunction (p=0.019). However, there was no association of ACE genotype or circulating ACE with central aortic blood pressure, aortic augmentation or pulse pressure amplification.

    Conclusion: Subjects with LV dysfunction have higher levels of circulating ACE compared to subjects with normal LV function. ACE might play a role in the pathogenesis of LV dysfunction and our data indicates a direct effect on the heart rather than affecting central blood pressure.

  • 8.
    Ljungberg, Liza
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Alehagen, Urban
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Kardiologiska kliniken US.
    Länne, Toste
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Thorax-kärlkliniken i Östergötland.
    Björck, Hanna
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet.
    De Basso, Rachel
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet.
    Dahlström, Ulf
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Kardiologiska kliniken US.
    Persson, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    The association between circulating angiotensin-converting enzyme and cardiovascular risk in the elderly: A cross-sectional study.2011Inngår i: jraas. Journal of the renin-angiotensin-aldosterone system, ISSN 1470-3203, E-ISSN 1752-8976, Vol. 12, nr 3, s. 281-289Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    INTRODUCTION: A polymorphism in the angiotensin-converting enzyme gene (ACE I/D polymorphism) has been associated with increased risk for cardiovascular disease (CVD). This polymorphism affects the level of circulating ACE, but there is great individual variation, even between those with the same genotype. Few previous studies have investigated the link between circulating ACE and cardiovascular risk. The aim of this study was to investigate this association, and to examine the relationship between ACE level, ACE genotype and CVD.

    MATERIALS AND METHODS: The study population consisted of 322 men and 350 women aged 69-87. Plasma ACE level was determined using enzyme-linked immunosorbent assay (ELISA), and ACE genotype was analysed using PCR followed by gel electrophoresis.

    RESULTS: In men, ACE levels increased with increasing number of cardiovascular risk factors (p = 0.003). There was a significant association in men between increased ACE level and both diabetes (p = 0.007) and smoking (p = 0.037).

    CONCLUSIONS: This study shows that cardiovascular risk factors (such as smoking and diabetes) are associated with higher levels of circulating ACE in men. High ACE levels may represent one of the cellular mechanisms involved in producing the vascular damage associated with cardiovascular risk factors.

  • 9.
    Ljungberg, Liza
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    De Basso, Rachel
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi.
    Alehagen, Urban
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Kardiologiska kliniken US.
    Björck, Hanna
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet.
    Persson, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Dahlström, Ulf
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Kardiologiska kliniken US.
    Länne, Toste
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Thorax-kärlkliniken i Östergötland.
    Impaired abdominal aortic wall integrity in elderly men carrying the angiotensin-converting enzyme D allele2011Inngår i: European Journal of Vascular and Endovascular Surgery, ISSN 1078-5884, E-ISSN 1532-2165, Vol. 42, nr 3, s. 309-316Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: A genetic polymorphism in the angiotensin-converting enzyme gene (ACE I/D polymorphism) has been associated with abdominal aortic aneurysm and a link between aortic aneurysm and aortic stiffness has been suggested. The aim of this study was to explore the links between ACE I/D polymorphism, circulating ACE, and abdominal aortic wall integrity as reflected by abdominal aortic wall stiffness.

    Material: The study population consisted of 406 subjects (212 men and 194 women) aged 70-88 years.

    Methods: The mechanical properties of the abdominal aorta were determined 3-4 cm proximal to the aortic bifurcation using a Wall Track System. ACE-genotype was determined by PCR followed by gel electrophoresis, and circulating ACE level was measured by ELISA.

    Results: Men carrying the ACE D allele had lower distensibility coefficient than II carriers (ID/DD 8.09 vs II 10.38, P=0.017). Multiple regression analyses showed additional associations between the ACE D allele and increased stiffness β as well as reduced cross-sectional compliance.

    Conclusion: This study showed that men carrying the ACE D allele have stiffer abdominal aortas compared to II carriers. Deranged abdominal aortic stiffness indicates impaired vessel wall integrity, which along with other local predisposing factors, may be of importance in aneurysmal disease.

  • 10.
    Ljungberg, Liza
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Hälsouniversitetet.
    Johan Östgren, Carl
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för samhällsmedicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Närsjukvården i västra Östergötland, Primärvården i västra länsdelen.
    Nyström, Fredrik H
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Endokrinmedicinska enheten.
    Länne, Toste
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Thorax-kärlkliniken i Östergötland.
    Associations of genetic polymorphisms in the renin-angiotensin system with central aortic and ambulatory blood pressure in type 2 diabetic patients2014Inngår i: jraas. Journal of the renin-angiotensin-aldosterone system, ISSN 1470-3203, E-ISSN 1752-8976, Vol. 15, nr 1, s. 61-68Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Patients with type 2 diabetes (T2D) are at high risk of developing hypertension and related cardiovascular disease. The renin-angiotensin system (RAS) plays a central role in regulation of blood pressure (BP). Accordingly, each component of this system represents a potential candidate in the etiology of hypertension. This study investigated the impact of polymorphisms within the RAS on ambulatory and central BP in T2D subjects. A cohort of 761 subjects (55-65 years) with T2D was studied. Ambulatory and central BP were measured, and ACE I/D genotype, angiotensinogen M235T, renin rs6693954 and ATR1-A1166C polymorphisms were analyzed. Women carrying the AA-genotype had lower 24-hour and day-time systolic and diastolic BP (pless than0.05), and lower night-time and central diastolic BP (pless than0.05), compared to T allele carriers. In men, the AA-genotype was instead associated with higher central diastolic BP (p=0.018) and higher augmentation index (p=0.016). Further, the associations between the renin rs6693954 SNP and diastolic BP were strongly gender dependent (p less than= 0.001). In T2D patients, there is a gender-dependent association of the renin rs6693954 SNP with central and ambulatory BP. Women carrying the renin rs6693954 AA-genotype may be protected against the higher BP seen in men with the same genotype.

  • 11.
    Ljungberg, Liza
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Persson, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    ACE GEnotype Determines Activity and Levels of Serum ACE but not Tissue ACE2007Inngår i: Atherosclerosis suppl, 2007, s. 1-Konferansepaper (Fagfellevurdert)
  • 12.
    Ljungberg, Liza
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Persson, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Effect of Nicotine and Nicotine Metabolites on Angiotensin-Converting Enzyme in Human Endothelial Cells2008Inngår i: Endothelium, ISSN 1062-3329, E-ISSN 1029-2373, Vol. 15, nr 5-6, s. 239-245Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Nicotine has been shown to induce endothelial dysfunction, which is an early marker of atherosclerosis. Nicotine undergoes extensive metabolism in the liver, forming a number of major and minor metabolites. There are very limited data on the effect of nicotine metabolites on the cardiovascular system. This study investigates the effects of nicotine and the nicotine metabolites, cotinine, cotinine-N-oxide, nicotine-1-N-oxide, norcotinine, trans-3-hydroxycotinine, on angiotensin-converting enzyme (ACE) in human endothelial cells. Cultured endothelial cells obtained from human umbilical cord vein (HUVECs) were stimulated with nicotine or nicotine metabolites in concentrations similar to those observed in plasma during smoking. ACE activity and expression were analyzed using commercial kits. The results showed that nicotine and nicotine metabolites can increase both activity and expression of ACE. However, a marked individual variation in the response to the drugs was observed. This variation was not associated with the ACE insertion/deletion polymorphism. Tobacco contains numerous chemical compounds, and the underlying cause for development of atherosclerosis in smokers is probably multifactorial. The results from this study could explain one cellular mechanism by which smoking exerts negative effect on the vascular system.

  • 13.
    Ljungberg, Liza
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Persson, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Effect of Tobacco Use on Angiotensin-Converting Enzyme in Human Endothelial Cells2008Konferansepaper (Annet vitenskapelig)
  • 14.
    Ljungberg, Liza
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Persson, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Nicotine and Nicotine metabolites increases ACE activity in human endothelial cells2006Inngår i: Scandinavian Cardiovascular Journal Suppl, 2006, s. 54-Konferansepaper (Fagfellevurdert)
  • 15.
    Ljungberg, Liza
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet.
    Persson, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Eriksson, Andreas
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Green, Henrik
    Linköpings universitet, Institutionen för medicin och hälsa, Klinisk farmakologi. Linköpings universitet, Hälsouniversitetet.
    Whiss, Per
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Effects of nicotine, its metabolites and tobacco extracts on human platelet function in vitro2013Inngår i: Toxicology in Vitro, ISSN 0887-2333, E-ISSN 1879-3177, Vol. 27, nr 2, s. 932-938Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Cigarette smoking is a leading cause of cardiovascular disease. The cardiovascular effects of smoking are probably multifactorial, including effects on platelets. Previous reports investigating the effects of nicotine and tobacco on platelet function are inconsistent.

    The present study investigated in vitro effects of nicotine, its major metabolites, tobacco extracts and extract of tobacco-free snuff on human platelets.

    None of the metabolites cotinine, cotinine-N-oxide, nicotine-1′-N-oxide or trans-3′-hydroxycotinine (0.1–10 μM) affected platelet aggregation or P-selectin expression. Nicotine (10 μM) weakly increased platelet aggregation, whereas trans-3′-hydroxycotinine (0.1 μM) and nicotine-1′-N-oxide (1–10 μM) weakly inhibited adhesion to fibrinogen. To elucidate the influence of other tobacco compounds, we investigated the impact of moist tobacco and smoke extracts on platelet function. Filtered extracts of oral snuff, cigarette smoke and tobacco free snuff inhibited platelet adhesion concentration-dependently. The inhibitory effects of tobacco extracts on platelet adhesion were independent of nicotine content and the nitric-oxide-pathway and not mediated through a platelet-nicotine-receptor.

    Taken together, tobacco extracts inhibit platelet activation during short-term in vitro challenge. As only limited effects of nicotine and nicotine metabolites were seen, the tobacco-induced platelet inhibition are likely induced by other compounds present in tobacco and tobacco free snuff.

  • 16.
    Ljungberg, Liza U.
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet.
    Alehagen, Urban
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Kardiologiska kliniken US.
    De Basso, Rachel
    Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet.
    Persson, Karin
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Dahlström, Ulf
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Kardiologiska kliniken US.
    Länne, Toste
    Linköpings universitet, Centrum för medicinsk bildvetenskap och visualisering, CMIV. Linköpings universitet, Institutionen för medicin och hälsa, Fysiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Thorax-kärlkliniken i Östergötland.
    Circulating angiotensin-converting enzyme is associated with left ventricular dysfunction, but not with central aortic hemodynamics2013Inngår i: International Journal of Cardiology, ISSN 0167-5273, E-ISSN 1874-1754, Vol. 166, nr 2, s. 540-541Artikkel i tidsskrift (Fagfellevurdert)
1 - 16 of 16
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