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Realities and prospects for pharmacological correction of «ADMA-eNOS

Author(s): M.V. Pokrovsky | N.G. Filipenko | M.V. Korokin | V.V. Gureyev | T.G. Pokrovsky | A.A. Barsuk | L.V. Korokina | E.V. Proskuryakova | N.V. Maltseva | O.V. Levashova | O.S. Gudyrev | A.S. Belous | O.S. Polyanskaya

Journal: Racionalʹnaâ Farmakoterapiâ v Kardiologii
ISSN 1819-6446

Volume: 6;
Issue: 6;
Start page: 882;
Date: 2010;
Original page

Keywords: endothelial dysfunction | preeclampsia | ADMA | eNOS.

Methylated analogs of L-arginine - asymmetric dimetilarginin (ADMA) and monometilarginin (L-NMMA) - are endogenous inhibitors of endothelial NO-synthase (eNOS). ADMA level in maternal plasma is increased in women with preeclampsia. The high level of ADMA is one of the predictors of preeclampsia. L-arginine increases the activity of eNOS and production of nitric oxide in the ADMA-similar model of L-NAME-induced endothelial dysfunction. ENOS activator (resveratrol), antioxidants, potentiated polyclonal antibodies to eNOS and others agents have been effective in this model. Studies of endotelioprotective activity in other ≪ADMA-eNOS-associated" experimental models of metabolic syndrome and homocysteine-induced, gipoestrogen-induced sepsis-induced endothelial dysfunction and endothelial dysfunction in postvaccinal vasculitis have been developed.
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