Compounds > 2-phenyl-4-4-5-5-tetramethylimidazoline-1-oxyl-3-oxide

2-phenyl-4-4-5-5-tetramethylimidazoline-1-oxyl-3-oxide and nitroaspirin

2-phenyl-4-4-5-5-tetramethylimidazoline-1-oxyl-3-oxide has been researched along with nitroaspirin* in 1 studies

Other Studies

1 other study(ies) available for 2-phenyl-4-4-5-5-tetramethylimidazoline-1-oxyl-3-oxide and nitroaspirin

Article	Year
A common pathway for nitric oxide release from NO-aspirin and glyceryl trinitrate. Biochemical and biophysical research communications, 2000, Jul-21, Volume: 274, Issue:1 NO-Aspirin (NCX-4016) releases nitric oxide (NO) in biological systems through as yet unidentified mechanisms. In LLC-PK1 kidney epithelial cells, a 5-h pretreatment with glyceryl trinitrate (GTN, 0.1-1 microM) significantly attenuated the cyclic GMP response to a subsequent challenge with both NO-aspirin or GTN. Similarly, NO-aspirin (10-100 microM) was found to induce tolerance to its own cyclic GMP stimulatory action and to that of GTN. In contrast, cyclic GMP stimulation by the spontaneous NO donor SIN-1, which releases NO independently of enzymatic catalysis, remained unimpaired in cells pretreated with GTN or NO-aspirin. The observed cross-tolerance between NO-aspirin and GTN cells indicates that bioactivation pathways of organic nitrates, which have been shown to involve cytochrome P450, may also be responsible for NO release from NO-aspirin. Prolonged treatment with NO-aspirin causes down-regulation of the cellular cyclic GMP response, suggesting that tolerance may occur during therapy with NO-aspirin. Topics: Animals; Aspirin; Cell Line; Cyclic GMP; Cyclic N-Oxides; Cytochrome P-450 Enzyme System; Dose-Response Relationship, Drug; Epithelial Cells; Free Radical Scavengers; Imidazoles; Kidney; Molsidomine; Nitric Oxide; Nitric Oxide Donors; Nitroglycerin; Protein Binding; Swine	2000

Article

Year

A common pathway for nitric oxide release from NO-aspirin and glyceryl trinitrate.

Biochemical and biophysical research communications, 2000, Jul-21, Volume: 274, Issue:1

NO-Aspirin (NCX-4016) releases nitric oxide (NO) in biological systems through as yet unidentified mechanisms. In LLC-PK1 kidney epithelial cells, a 5-h pretreatment with glyceryl trinitrate (GTN, 0.1-1 microM) significantly attenuated the cyclic GMP response to a subsequent challenge with both NO-aspirin or GTN. Similarly, NO-aspirin (10-100 microM) was found to induce tolerance to its own cyclic GMP stimulatory action and to that of GTN. In contrast, cyclic GMP stimulation by the spontaneous NO donor SIN-1, which releases NO independently of enzymatic catalysis, remained unimpaired in cells pretreated with GTN or NO-aspirin. The observed cross-tolerance between NO-aspirin and GTN cells indicates that bioactivation pathways of organic nitrates, which have been shown to involve cytochrome P450, may also be responsible for NO release from NO-aspirin. Prolonged treatment with NO-aspirin causes down-regulation of the cellular cyclic GMP response, suggesting that tolerance may occur during therapy with NO-aspirin.

Topics: Animals; Aspirin; Cell Line; Cyclic GMP; Cyclic N-Oxides; Cytochrome P-450 Enzyme System; Dose-Response Relationship, Drug; Epithelial Cells; Free Radical Scavengers; Imidazoles; Kidney; Molsidomine; Nitric Oxide; Nitric Oxide Donors; Nitroglycerin; Protein Binding; Swine

2000