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Last Updated: 3 years ago

Possible Interaction: Ng-Nitroarginine Methyl Ester and Vitamin C

Research Papers that Mention the Interaction

L-NAME also abrogated the increase in NOx and improvement of LV function and the infarct size-limiting effect induced by AA or NAC in the diabetic heart.
Free radical research  •  2011  |  View Paper
Vitamin C + L-NAME also induced significant decrease in TBARS production.
General physiology and biophysics  •  2011  |  View Paper
The application of l-NAME partially and temporarily reversed the anticonvulsant effects of ascorbic acid.
The protective effect of ascorbic acid against epileptiform activity was partially and temporarily reversed by nonspecific nitric oxide synthase inhibitor l-NAME , but not selective neuronal nitric oxide synthase inhibitor 7-NI, indicating that ascorbic acid needs endothelial-NOS/NO route to decrease penicillin-induced epileptiform activity.
Seizure  •  2010  |  View Paper
Furthermore, simultaneous injection of L-NAME (20.0 mg/Kg) and treatment with α-tocopherol and ascorbic acid prevented these effects.
Metabolic Brain Disease  •  2006  |  View Paper
Nw‐nitro‐L‐arginine methyl ester (l‐NAME, 10 mmol/L) significantly attenuated the vasodepressor effects of quercetin and ascorbic acid , raising the responses to PE to a level similar to that observed in the control SHR tissues.
Clinical and experimental pharmacology & physiology  •  2006  |  View Paper
In these groups, vitamin C improved the response to acetylcholine and restored the inhibition by L-NAME.
Arteriosclerosis, thrombosis, and vascular biology  •  2003  |  View Paper
Ascorbic acid was highly effective in reacting with L-NAME to produce NO, while glutathione, NADPH, and NADH were much less effective.
Nitric oxide : biology and chemistry  •  2003  |  View Paper
L-NAME significantly inhibited ethanol-induced release of AA , while SNP only had a transient inhibitory effect on the ethanol-induced release of AA.
Toxicology letters  •  2003  |  View Paper
Indomethacin, but not L-NAME , partially inhibited the relaxing effect of ascorbic acid.
General pharmacology  •  1997  |  View Paper
Endothelium-dependent relaxation was resistant to L-NAME and enhanced by ascorbic acid , which restored also the inhibitory effect of L-NAME , suggesting a ROS-dependent reduction of NO availability in HFD vessels.
Front. Pharmacol.  •  2018  |  View Paper