Antagonistic action of imidazolineoxyl N-oxides against endothelium-derived relaxing factor/.bul.NO (nitric oxide) through a radical reaction

Akaike, Takaaki; Yoshida, Masaki; Miyamoto, Yukio; Sato, Keizo; Kohno, Masahiro; Sasamoto, Kazumi; Miyazaki, Kensuke; Ueda, Shoichi; Maeda, Hiroshi

doi:10.1021/bi00054a013

Cited by 562 publications

(344 citation statements)

References 26 publications

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“…These data suggest that NO increases synaptic GABA release in the PAG, and that the site of action of NO is most likely to locate at presynaptic GABAergic terminals (Sulzer and Pothos, 2000). Furthermore, the effects of SNAP and L-arginine on mIPSCs of the dl-PAG were completely eliminated by the specific NO scavenger carboxy-PTIO (Akaike et al, 1993) and the specific nNOS inhibitor TRIM (Handy et al, 1995), respectively (Fig. 1&2).…”

Section: Discussionmentioning

confidence: 74%

Role of GABA receptors in nitric oxide inhibition of dorsolateral periaqueductal gray neurons

Xing

2008

Neuropharmacology

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Nitric oxide (NO) affects neuronal activity of the midbrain periaqueductal gray (PAG). The purpose of this report was to investigate the role of GABA receptors in NO modulation of neuronal activity through inhibitory and excitatory synaptic inputs within the dorsolateral PAG (dl-PAG). First, spontaneous miniature inhibitory postsynaptic currents (mIPSCs) and excitatory postsynaptic currents (mEPSCs) were recorded using whole cell voltage-clamp methods. Increased NO by either S-nitroso-N-acetyl-penicillamine (SNAP, 100 μM) or L-arginine (50 μM) significantly augmented the frequency of mIPSCs of the dl-PAG neurons without altering their amplitudes or decay time constants. The effects were eliminated after bath application of carboxy-PTIO (NO scavenger), and 1-(2-trifluorom-ethylphenyl) imidazole (NO synthase inhibitor). In contrast, SNAP and L-arginine did not alter mEPSCs in dl-PAG neurons. However the frequency of mEPSCs was significantly increased with prior application of the GABA B receptors antagonist, CGP55845. In addition, NO significantly decreased the discharge rate of spontaneous action potentials in the dl-PAG neurons and the effect was reduced in the presence of the GABA A receptor antagonist, bicuculline. Our data show that within the dl-PAG NO potentiates the synaptic release of GABA, while NO-induced GABA presynaptically inhibits glutamate release through GABA B receptors. Overall, NO suppresses neuronal activity of the dl-PAG via a potentiation of GABAergic synaptic inputs and via GABA A receptors.

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Section: Discussionmentioning

confidence: 74%

Role of GABA receptors in nitric oxide inhibition of dorsolateral periaqueductal gray neurons

Xing

2008

Neuropharmacology

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“…It is known that NO specifically reduces PTIO into a different nitroxide radical, 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl (PTI), and the conversion of the ESR signals of PTIO into those of PTI indicates generation of NO [15]. Thus, N0 2 (40 nmol) in air was introduced into chloroform containing 40 nmol PTIO and 7.2 nmol ß-carotene.…”

Section: Resultsmentioning

confidence: 99%

β‐Carotene effectively scavenges toxic nitrogen oxides: nitrogen dioxide and peroxynitrous acid

Kikugawa¹,

Hiramoto²,

Tomiyama³

et al. 1997

FEBS Letters

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ß-Carotene absorbed 2 equimolar amounts of N0 2 accompanying the complete destruction of ß-carotene. Electron spin resonance study using 2-phenyl-4,4,5,5-tetramethylimidazoline-3-oxide-l-oxyl revealed that no significant amounts of NO were released by the interaction. Nitrogen atoms derived from N0 2 were tightly bound to the ß-carotene molecules. Destruction of ß-carotene was inhibited little by a-tocopherol and polyunsaturated fatty esters, and slightly by ascorbyl palmitate, indicating that ß-carotene was a more effective scavenger of N0 2 . ONOOH/ONOO -and 3-morpholinosydononimine similarly destroyed ß-carotene. The results suggest that ß-carotene contributes to the prevention of cytotoxicity and genotoxicity of N0 2 and ONOOH/ONOO" derived from NO.

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“…Furthermore, intravenous or intraperitoneal injection and oral treatment of tempol reduces arterial pressure in SHR (15,25). Although the radical form of NO can react with tempol and, as a result, lose its physiological activity (26), tempol can restore NO-dependent relaxation in the presence of oxidant stress (27). From these results, we hypothesized that the central infusion of tempol could inhibit the degeneration of NO by superoxide, thereby preserving the inhibitory action of NO in the central nervous system, and, as a consequence, reducing blood pressure in SHR.…”

Section: Discussionmentioning

confidence: 99%

Central Infusion of L-Arginine or Superoxide Dismutase Does Not Alter Arterial Pressure in SHR.

et al. 2000

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Antagonistic action of imidazolineoxyl N-oxides against endothelium-derived relaxing factor/.bul.NO (nitric oxide) through a radical reaction

Cited by 562 publications

References 26 publications

Role of GABA receptors in nitric oxide inhibition of dorsolateral periaqueductal gray neurons

Role of GABA receptors in nitric oxide inhibition of dorsolateral periaqueductal gray neurons

β‐Carotene effectively scavenges toxic nitrogen oxides: nitrogen dioxide and peroxynitrous acid

Central Infusion of L-Arginine or Superoxide Dismutase Does Not Alter Arterial Pressure in SHR.

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