nitroarginine has been researched along with hydrazine* in 2 studies
2 other study(ies) available for nitroarginine and hydrazine
| Article | Year |
|---|---|
Effect of hydrazine upon vitamin B12-dependent methionine synthase activity and the sulphur amino acid pathway in isolated rat hepatocytes.
The effect of the industrial chemical, hydrazine (4-12 mM), on methionine synthase (EC 2.1.1.13) activity and levels of the sulphur amino acids homocysteine, cysteine, and taurine as well as GSH were investigated in vitro in isolated rat hepatocyte suspensions and monolayers in order to explain some of the adverse in vivo effects of hydrazine. None of the concentrations of hydrazine were overtly cytotoxic in hepatocyte suspensions (measured as lactate dehydrogenase [LDH] leakage) after 3 hr. However, after 24 hr in culture cells treated with 12 mM, hydrazine showed a significant increase in LDH leakage. Methionine synthase activity was reduced by hydrazine (8 and 12 mM) in suspensions (by 45 and 55%, after 3 hr) and monolayers (12 mM; 65-80% after 24 hr). This was not due to nitric oxide production and the inhibitor of nitric oxide synthase, Nomega-nitro-L-arginine, failed to protect against the hydrazine-induced loss of ATP and GSH and the reduction in urea synthesis at 24 hr. Homocysteine export was increased by 6 mM hydrazine, and total taurine content of treated cells was increased by 12 mM hydrazine. Thus, hydrazine was found to have several important and possibly deleterious effects on some parts of the sulphur amino acid pathway. Topics: 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; Amino Acids, Sulfur; Animals; Carcinogens; Cell Survival; Culture Media; Cysteine; Cytosol; Enzyme Inhibitors; Homocysteine; Hydrazines; Liver; Male; Nitroarginine; Rats; Rats, Wistar; Taurine; Vitamin B 12 | 1999 |
Inhibitory mechanism of N(G)-nitro-L-arginine on acetylcholine-induced depressor responses in dogs.
The significance of the blood pressure elevation caused by N(G)-nitro-L-arginine (L-NNA) to inhibitory mechanism of the drug on depressor responses to acetylcholine in anesthetized dogs was investigated. L-NNA (50 mg kg(-1), i.v.) elevated blood pressure to a plateau of 30-50 mm Hg above baseline level and shifted the dose-response curve for acetylcholine-induced responses to the right by about 70-fold. Prevention by hydralazine (1 mg kg(-1), i.v.) of the blood pressure elevation over baseline level caused by L-NNA attenuated the inhibitory effect of L-NNA on the responses to acetylcholine. Intravenous neostigmine (30 microg kg(-1) bolus followed by 15 microg kg(-1) min(-1)) attenuated the inhibitory effect of L-NNA. The magnitude of the rightward shift in the dose-response curve for carbachol-induced depressor responses was only 3-fold. These results suggest that the accelerated acetylcholine metabolism by blood pressure elevation contributes to a considerable degree to the inhibitory mechanism of L-NNA. Topics: Acetylcholine; Animals; Atropine; Blood Pressure; Carbachol; Carcinogens; Cholinergic Agents; Cholinesterases; Dogs; Dose-Response Relationship, Drug; Enzyme Inhibitors; Female; Hydrazines; Male; Neostigmine; Nitroarginine; Vasodilator Agents | 1999 |