Wynik wyszukiwania w bazie Polska Bibliografia Lekarska GBL

Zapytanie: KOZLOVSKI
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Tytuł oryginału: Flavonoids and nitric oxide synthase.
Autorzy: Olszanecki R[afał], Gębska A[nna], Kozlovski V. I., Gryglewski R. J.
Źródło: J. Physiol. Pharmacol. 2002: 53 (4) p. 1 s.571-584, il., bibliogr. 38 poz.
Sygnatura GBL: 302,092

Hasła klasyfikacyjne GBL:
  • kardiologia

    Typ dokumentu:
  • praca doświadczalna

    Wskaźnik treści:
  • zwierzęta
  • myszy
  • Świnki morskie
  • in vitro

    Streszczenie angielskie: Induction of NOS-2 in macrophages and smooth muscles within vascular wall with concomittant suppression of endothelial NOS-3 activity is considered to be a hallmark of vascular inflammation that triggers atherogenesis. Accordingly, drugs designed to reverse these changes should not only support vaning function of NOS-3 but also suppress proinflammatory NO production by NOS-2. It means that using selective inhibitors of induction of NOS-2 (they spare ex definitione constitutive activity of NOS-3) is a more rational approach than using "selective" inhibitors of activity to previously induced NOS-2. First of all, those drugs are never sufficiently selective. In our work we tried to identify inhibitors of NOS-2 induction within the group of flavonoids, known stimulators of NOS-3 with putative antiatherogenic effects. Representatives of four main groups of flavonoids: flavonols (kaempferol, quercetin, rutin), flavones (apigenin, primuletin), flavanols (catechine) and flavones (hesperetin, hesperidin, naringenin) were tried on NOS-2 induction and activity in the in vitro model of LPS-treated macrophages (cell line J774.2). While none of these compounds inhibited activity of NOS-2, all with unexpectedly scattered potencies inhibited induction of NOS-2 protein in LPS-treated J774.2 cells, as evidenced by Western blotting technique. Subsequently, RT-PCR and Northern blotting methods revealed that so far the most potent compounds, kaempferol and apigenin, at micromolar concentrations did inhibit NOS-2 induction ...


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    Tytuł oryginału: No-dependent vasodilation induced by nebivolol in coronary circulation is not mediated by á-adrenoceptors or by 5 HT1A-receptors.
    Autorzy: Chłopicki S[tefan], Kozlovski V[alery] I., Gryglewski R. J.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (4 p. 1) s.615-624, il., bibliogr. 19 poz., sum.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • kardiologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • Świnki morskie
  • in vitro

    Streszczenie angielskie: Nebivolol is a unique á1-adrenoceptor antagonist which possesses peripheral vasodilator properties dependent on endothelial NO. Nebivolol-induced release of NO was attributed to its L stereoisomer and to its ability to stimulate endothelial á2, á3 adrenoceptors or 5 HT1A receptors. Here, in the isolated guinea pig heart we analysed coronary vasodilator potency of L- and D-nebivolol and a possible role of á2, á3 adrenoceptors and 5-HT1A receptors in nebivolol-induced vasodilation. Surprisingly, we ound that not only L-nebivolol (3-30x10**-6 M) but also D-nebivolol (3-30x10**-6 M) induced coronary vasodilation, and both responses were inhibited by L-NAME (10**-4 M). In contrast with the stereoisomers of nebivolol, atenolol at the equimolar concentrations did induce slight casoconstriction. The nonselective á1/á2-adrenoceptor antagonist - nadolol (10-5 M). The selective á3-adrenoceptor antagonist - L 748337 (10**6 M) and the 5 HT1A receptor antagonist - NAN 190 (5 x 10**-6 M), none of them inhibited coronary vasodilation induced by D- and L-nebivolol. In summary, in the isolated guinea pig heart both D- and L-nebivolol act as coronary vasodilators. Coronary vasodilation induced by stereoisomers of nebivolol is mediated by endothelium-derived NO and does not depend on á2, á3 adrenoceptors or 5 HT1A receptors.


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    Tytuł oryginału: Paradoxical augumentation of bradykinin-induced vasodilatation by xanthine/xanthine oxidase-derived free radicals in isolated guinea pig heart.
    Autorzy: Olszanecki R[afał], Kozlovski V[alery] I., Chłopicki S[tefan], Gryglewski R. J.
    Źródło: J. Physiol. Pharmacol. 2002: 53 (4 p. 1) s.689-699, il., tab., bibliogr. 42 poz.
    Sygnatura GBL: 302,092

    Hasła klasyfikacyjne GBL:
  • farmacja
  • kardiologia

    Typ dokumentu:
  • praca doświadczalna
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • zwierzęta
  • Świnki morskie
  • in vitro

    Streszczenie angielskie: Increased generation of reactive oxygen species contribute to endothelial dysfunction in atherosclerosis, hypertension and heart failure. Recently, it was suggested that bursts of superoxide anions may inactivate endothelial surface-bound enzymes such as angiotensin converting enzyme (ACE). Here, we tested effects of xanthine/xanthine oxidase-derived superoxide anions on vascular responses and ACE activity in the isolated guinea pig heart. We anlysed effects of intracoronary infusion of low concentration of xanthine oxidase (10 mU/ml) in the presence of xanthine (0,5 mM) (X/XO) on bradykinin, other endothelium-dependent and independent vasodilators (acetylcholine, ADP, SNAP), as well as vasoconstrictor responses to angiotensin I and angiotensin II. Surprisingly, X/XO significantly augumented coronary response to bradykinin without an effect on response to ADP, acetylcholine, SNAP, angiotensin I and angiotensin II. In contrast, inhibition of ACE by perindoprilate (100 nM) resulted in augumentation of bradykinin-induced vasodialidation as well as diminution of angiotensin I-evoked vasoconstriction without an influence on other responses. In summary, in the isolated guinea pig heart, X/XO-derived free radicals selectivity augumented coronary vasodilator response to bradykinin, which cannot be explained by X/XO-induced derangement of ACE. The mechanism of this paradoxical phenomenon, which might represent a defensive response of the coronary circulation to oxidative stress requires further investigations.

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