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Irwin C et al. – Nitric oxide (NO)–mediated inhibition of platelet function occurs primarily through elevations in cGMP, although cGMP–independent mechanisms such as S–nitrosylation have been suggested as alternative NO–signaling pathways. S–nitrosylation of platelet proteins in response to exogenous NO may act as a potentially important cGMP–independent signaling mechanism for controlling platelet adhesion.

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