Key result
Following vascular injury, cellular methylarginines increased approximately 4-fold, reaching levels sufficient to significantly inhibit endothelial NO synthase and impair vascular relaxation.
Endogenous methylarginines like ADMA and l-NMMA accumulate in endothelial cells and, at levels seen in disease states such as vascular injury, significantly inhibit eNOS and impair vascular relaxation.
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Methylarginines may drive post-injury endothelial dysfunction; animal data leave open human relevance and therapeutic targeting.
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Cardounel et al. (2006) studied Vascular dysfunction. Endogenous methylarginines (ADMA and l-NMMA) vs. Normal physiological levels was evaluated on Endothelial NO production and vascular relaxation. Following vascular injury, cellular methylarginines increased approximately 4-fold, reaching levels sufficient to significantly inhibit endothelial NO synthase and impair vascular relaxation.
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