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Tytuł oryginału: Increased nitric oxide bioavailability in endothelial cells contributes to the pleiotropic effect of cerivastatin.
Autorzy: Kalinowski Leszek, Dobrucki Lawrence W., Brovkovych Viktor, Maliński Tadeusz
Źródło: Circulation 2002: 105 (8) s.933-938, il., bibliogr. 17 poz.
Sygnatura GBL: 311,033

Hasła klasyfikacyjne GBL:
  • farmacja
  • kardiologia

    Typ dokumentu:
  • praca doświadczalna
  • praca opublikowana za granicą
  • tytuł obcojęzyczny

    Wskaźnik treści:
  • ludzie
  • in vitro

    Streszczenie angielskie: Although statins preserve endothelial function by reducing serum cholesterol levels, it has been suggested they may also stimulate nitric oxide (NO) synthase in endothelium with concurrent increase in superoxide (O2-) generation, leading to impairment of NO activity. Therefore, measurements of biologically active NO and O2 - in endothelium after exposure to the HMG-CoA reductase inhibitor cerivastatin were undertaken to evaluate its potential effect on NO biological activity. Methods and Results - Highly sensitive electrochemical NO and O2 - microsensors were placed near the surface of a single human umbilical vein endothelial cell, and the kinetics of NO and O2 - release were recorded in vitro. Cerivastatin demonstrated a time-dependent effect on NO release in endothelial cels. The initial release (approximately the first 3 minutes) was concentration-dependent (0.01 to 10 ćmol/L) and was similar to that observed for typical NO synthase agonists calcium ionophore or acetylcholine. Cerivastatin stimulated NO release at a favorable rate and scavenged O2-, which led to the preservation of the active concentration of NO. The sustained effect (after ÷ 6 hours) of cerivastatin on endothelium was associated with an ÷ 35 p.c. increase in NO release as compared with the initial effect. In contrast to the initial effect, the sustained effect of cerivastatin was shown at concenrations ÷ 100-fold lower and was dependent on inhibition of endothelial HMG-CoA reductase. Conclusions - These data provide direct evidence to prove that in the presence of cerivastatin, the NOS system in endothelium operates with high efficiency toward increasing NO activity by activation of NO release and by concurrent inactivation of O2-.

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