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    Wyświetlanie 1-2 z 2
    Tytuł:
    Metabolism of bradykinin in aorta of hypertensive rats
    Autorzy:
    Bujak-Giżycka, Beata
    Olszanecki, Rafał
    Madej, Józef
    Suski, Maciej
    Gębska, Anna
    Korbut, Ryszard
    Powiązania:
    https://bibliotekanauki.pl/articles/1039915.pdf
    Data publikacji:
    2011
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    bradykinin
    angiotensin converting enzyme
    mass spectrometry
    bioactive peptides
    Opis:
    Alterations in the formation and metabolism of bradykinin (Bk) are hypothesized to play a role in the pathophysiology of hypertension, atherosclerosis and vascular complications of diabetes. However, despite its prominent role in cardiovascular regulation, studies on bradykinin have been limited by various difficulties in accurate measurements of this peptide in biological samples. In this study, using the LC-ESI-MS method we estimated the conversion of exogenous Bk to its main metabolites - Bk-(1-5) and Bk-(1-7) - in endothelial cell culture and in fragments of aorta of normotensive (WKY) and hypertensive rats (SHR). The effects of angiotensin converting enzyme (ACE) and neutral endopeptidase (NEP) inhibitors were more pronounced in SHR: perindoprilat inhibited Bk-(1-5) formation by 49 % and 76 % in WKY and SHR rats, respectively, and tiorphan tended to decrease formation of Bk-(1-5) in both groups of animals. The degradation of bradykinin and generation of both metabolites were significantly higher in the aorta of SHR rats than in WKY controls. Our results show that even in relatively early hypertension (in 4-month old SHR rats) inactivation of Bk by aorta wall is enhanced.
    Źródło:
    Acta Biochimica Polonica; 2011, 58, 2; 199-202
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Carrier-state of D allele in ACE gene insertion/deletion polymorphism is associated with coronary artery disease, in contrast to the C677→T transition in the MTHFR gene.
    Autorzy:
    Żak, Iwona
    Niemiec, Paweł
    Sarecka, Beata
    Balcerzyk, Anna
    Ciemniewski, Zbigniew
    Rudowska, Ewa
    Dyląg, Stanisław
    Powiązania:
    https://bibliotekanauki.pl/articles/1043632.pdf
    Data publikacji:
    2003
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    angiotensin converting enzyme gene (ACE)
    coronary artery disease
    methylenetetrahydrofolate reductase gene (MTHFR)
    polymorphisms
    Opis:
    Angiotensin I-converting enzyme (ACE), which plays an important role in blood pressure regulation, and methylenetetrahydrofolate reductase (MTHFR) involved in homocysteine metabolism belong to a large group of polypeptides which may be potential risk factors for atherosclerosis and coronary artery disease (CAD). To assess whether polymorphisms of the genes encoding these peptides are associated with CAD in Silesian we conducted a study among 68 individuals suffering from CAD (including 52 cases after myocardial infarction), 51 subjects with positive family history of CAD and 111 controls. We analysed the distribution of genotypes and allele frequencies of the insertion/deletion (I/D) polymorphism in the ACE gene using PCR amplification, and the C677→T polymorphism in the MTHFR gene using PCR-RFLP analysis. We found that D allele frequency was significantly higher in CAD patients (61%) than in controls (43%) (P = 0.001, OR = 2.06). The D allele carriers (DD + ID genotypes) were more frequent in the CAD patients (85%) compared to control group (65%) (P = 0.003, OR = 3.14), whereas the familial CAD risk group shows the highest frequency of the ID genotype (57% vs 43% in controls). In contrast, the MTHFR polymorphism does not seem to be associated with the disease. Our data indicate that in Silesian CAD patients the disease is strongly associated with carrier-state of the ACE D allele, but not with the C677→T transition in the MTHFR gene.
    Źródło:
    Acta Biochimica Polonica; 2003, 50, 2; 527-534
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-2 z 2

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