Blockade of Retinal NMDA Receptors by Sodium Nitroprusside Is Probably Due to Nitric Oxide Formation
نویسندگان
چکیده
منابع مشابه
Nitric Oxide-Induced Blockade of NMDA Receptors
We studied the effects of nitric oxide (NO)-producing agents on N-methyl-D-aspartate (NMDA) receptor activation in cultured neurons. 3-Morpholino-sydnonimine (SIN-1) blocked both NMDA-induced currents and the associated increase in intracellular Ca2+. The actions of SIN-1 were reversible and suppressed by hemoglobin. A degraded SIN-1 solution that did not release NO was unable to block NMDA rec...
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Nitric oxide (NO) and NO donors were among the first reported inducers of the tissue-protective protein heme oxygenase-1 (HO-1) with a potential for eventual use in humans. Besides other clinically established NO releasing drugs, sodium nitroprusside (SNP) has frequently been employed as an experimental tool to explore effects of NO on HO-1 and other biological targets. In this issue of Molecul...
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Nitric oxide (NO) may play an important role in regulating retinal neuronal survival. While the precise impact of NO mechanisms on retinal neurons remains to be elucidated, it has been reported that low doses of NO may have a neuroprotective effect against N-methyl-D-aspartate (NMDA)-induced retinal neurotoxicity. Dopamine has also been recognized to have neuroprotective actions. Retinal dopami...
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The role of vascular smooth muscle inward rectifier K+ (K(IR)) channels in the mechanisms underlying vasodilation is still unclear. The hypothesis that K(IR) channels are involved in sodium nitroprusside (SNP)-induced dilation of rat-tail small arteries was tested. SNP relaxed tail small arteries with an EC50 of 2.6x10(-8) mol/L. Endothelium removal did not attenuate this effect. Vessel pretrea...
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Nitric oxide (NO) is a potent extracellular and intracellular physiological messenger. However, NO liberated in excessive amounts can be involved in macromolecular and mitochondrial damage in brain aging and in neurodegenerative disorders. The molecular mechanism of its neurotoxic action is not fully understood. Our previous data indicated involvement of NO in the release of arachidonic acid (A...
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ژورنال
عنوان ژورنال: Japanese Journal of Pharmacology
سال: 1993
ISSN: 0021-5198
DOI: 10.1254/jjp.62.49