Key result
ADMA is a weak competitive inhibitor of recombinant endothelial nitric oxide synthase (eNOS) with an IC50 of approximately 12 μM, suggesting physiological concentrations are unlikely to cause significant endothelial dysfunction.
Population
in vitro and in vivo models of endothelial nitric oxide synthase (eNOS) activity
Design
Review
Authors
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Challenges prevailing eNOS inhibition hypothesis for ADMA; leaves open alternative mechanisms for its cardiovascular risk associations.
Effect estimate: Ki 3.9 μM, IC50 12 μM
The cardiovascular risk associated with ADMA is likely due to unrecognized biological actions rather than direct inhibition of eNOS, challenging the prevailing hypothesis.
Dimitrios Tsikas (2017) studied this question. Asymmetric dimethylarginine (ADMA) vs. Absence of ADMA was evaluated on Inhibition of recombinant bovine eNOS activity (Ki 3.9 μM, IC50 12 μM). ADMA is a weak competitive inhibitor of recombinant endothelial nitric oxide synthase (eNOS) with an IC50 of approximately 12 μM, suggesting physiological concentrations are unlikely to cause significant endothelial dysfunction.
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