| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2551722 | Life Sciences | 2012 | 6 Pages |
Abstract
These results suggest that during inflammation when both ACh and high levels of fibrinogen are present, NO delivery by erythrocytes might be compromised by their NO scavenging ability that acts as a compensatory mechanism against the overproduced NO by endothelial inducible nitric oxide synthase.
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Authors
C. Saldanha, T. Freitas, J.P. Almeida,