Effect of FK409, a Novel Nitric Oxide Donor, on Acute Experimental Myocardial Ischemia

Isono, Toyokazu; Sato, Natsuki; Koibuchi, Yasushi; Sakai, Shigeru; Yamamoto, Takao; Ozaki, Reiko; Mori, Jo; Kohsaka, Masanobu; Ohtsuka, Minoru

doi:10.1254/jjp.62.411

Cited by 22 publications

(5 citation statements)

References 29 publications

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“…16) Another study confirmed that the Ca 2ϩ channel blockers have neuroprotective potential against high potassium-or glutamate-inducedcell death in neuronal cell cultures. 17) Surprisingly, in the present study, we did not find the same effect of nimodipine against SNP-induced neurotoxicity.…”

Section: Discussioncontrasting

confidence: 94%

Nitric Oxide Donor Sodium Nitroprusside Induces Neurotoxicity in Cerebellar Granular Cell Culture in Rats by an Independent Mechanism from L-Type or Dantrolene-Sensitive Calcium Channels.

Gepdíremen

Hacımüftüoğlu

Büyükokuroğlu

et al. 2002

Biological & Pharmaceutical Bulletin

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Nitric oxide (NO) plays a dual role (neuroprotection and neurotoxicity) in cerebral ischemia. As a neurotoxin, NO may mediate the ischemic excitotoxic brain injury induced by glutamate release and NMDA receptor overactivation. On the other hand, as a signalling molecule, NO may induce an increase in blood perfusion of ischemic penumbra in the early stages of cerebral ischemia. 1) NO is also a signalling molecule involved in events crucial to neuronal cell function such as neurotransmitter release, gene transcription and neurotoxicity.2) The mechanisms proposed for NO-mediated neurotoxicity include inactivation of the mitochondrial respiratory chain,3) S-nitrosylation of glyceraldehyde-3-phosphate dehydrogenase, 4) inhibition of cis-aconitase, 5) activation of poly (ADP-ribose) synthase, and DNA damage, 6) most of which can be mediated by the formation of nitroso compounds by cellular components. An important role for intracellular calcium in oxidant-induced cell death has been suggested by some, 7) yet this proposal remains controversial. On the one hand, it has been suggested that an increase in free Ca 2ϩ is nothing more than a late event associated with loss of membrane integrity and does not contribute appreciably to oxidant-induced cell death. 8) On the other hand, it has been proposed that an early increase in intracellular free Ca 2ϩ exacerbates oxidative stress, damages mitochondria, activates Ca 2ϩ -dependent degradative enzymes, and disrupts the cytoskeleton, all of which play a central role in oxidant-induced cell death.9) The endoplasmic reticulum is the major intracellular Ca 2ϩ storage site. 8) Oxidants, sulfhydryl active agents, and free radicals also inhibit Ca 2ϩ -ATPases and release Ca 2ϩ from the endoplasmic reticulum, suggesting that endoplasmic reticulum Ca 2ϩ could play a role in oxidant toxicity.10)The present study investigates the possible role of intracellular and extracellular Ca 2ϩ currents in sodium nitroprusside (SNP)-induced neurotoxicity in rat cerebellar granular cell cultures. MATERIALS AND METHODSPrimary cultures of cerebellar granule cells were prepared from 1-d-old newborn Sprague-Dawley rats as previously described by Xu and Wojcik.11) Briefly, newborn rats were decapitated and the cerebellum was removed. It was suspended in 5 ml of calcium-free Hank's balanced salt solution (HBSS, Sigma Chemical, St. Louis, MO, U.S.A.) containing 2 ml of trypsin-EDTA (0.25% trypsin-0.02% EDTA, Biol Ind, Haemek, Israel) at 37°C for 40 min. Trypsin digestion was ended adding by 10 ml of HBSS containing deoxyribonuclease type 1 (120 unit/ml, Sigma Chemical). After 3 min of centrifugation at 800 rpm, the resulting pellets were suspended. The bases of 25 cm 3 polypropylene tissue culture flasks were covered with poly-D-lysine. Twenty-four hours before the experiment, poly-D-lysine 0.1 mg/ml, 30000-70000 MW, was dissolved in phosphate-buffered saline (PBS) and the flask bases were filled with the same solution. After standing 5 min at room temperature, the solution was vacuumed and left to dry in...

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Section: Discussioncontrasting

confidence: 94%

Nitric Oxide Donor Sodium Nitroprusside Induces Neurotoxicity in Cerebellar Granular Cell Culture in Rats by an Independent Mechanism from L-Type or Dantrolene-Sensitive Calcium Channels.

Gepdíremen

Hacımüftüoğlu

Büyükokuroğlu

et al. 2002

Biological & Pharmaceutical Bulletin

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“…The different effects of Nif and Nic on MAP-or PCP-induced abnormal behaviors are somewhat difficult to interpret since the pharmacological potencies of 1,4-DHP antagonists on high K-evoked VSCC activity seen in the brain neural cell body are similar [28]. It has recently been reported that the presence of an L-type subunit was identified in an in vitro study [29].…”

Section: Discussionmentioning

confidence: 99%

Differentiation of the Inhibitory Effects of Calcium Antagonists on Abnormal Behaviors Induced by Methamphetamine or Phencyclidine

Hori¹,

Takeda²,

Tsuji³

et al. 1998

Pharmacology

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The abnormal behaviors induced by methamphetamine (MAP: 1 mg/kg) or phencyclidine (PCP: 10 mg/kg) were measured using behavioral analysis following the microinjection of one of three calcium (Ca) antagonists (nifedipine: Nif, nicardipine: Nic and flunarizine: Flu) into the rat caudate putamen or amygdala. The intraperitoneal administration of MAP or PCP induced abnormal behaviors in a time-dependent manner; the maximum locomotor activity was measured 30–45 min after the administration of MAP or PCP. This hyperactivity was sustained for more than 2 h. Following microinjection of these Ca antagonists into the caudate putamen, each showed a different pattern of inhibition on MAP- or PCP-induced abnormal behaviors. Nic and Flu were effective at reducing these abnormal behaviors, in contrast, Nif was ineffective. In particular, the inhibitory effect of Nic was stronger than that of Flu. Microinjection of these Ca antagonists into the amygdala did not show any reductive effect on the hyperactivity induced by MAP or PCP. These results demonstrate that these Ca antagonists have different pharmacological properties and that both L- and T-type Ca²⁺ channels modulate the dopamine release in the rat caudate putamen. These results further lead us to suggest the presence of a subtype of L-type Ca²⁺ channels in the caudate putamen.

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“…Acutely, nitric oxide administration to reperfused ischemic tissues will result in stimulation of vessel wall and circulating platelet and neutrophil cGMP levels. This will result in increased blood flow and oxygen delivery to tissues, as well as an alteration in shear forces on the vessel wall, critical for regulating inflammatory cell-vessel wall interactions and secondary gene expression events (112). The translocation of P-selectin to the platelet surface or the function of P-selectin becomes inhibited by • NO as well, resulting in attenuation of platelet-neutrophil aggregation and secondary "downstream" inflammatory cell-derived oxidant stress to the vasculature.…”

Section: Inflammation and • Nomentioning

confidence: 99%

Nitric Oxide Regulation of Tissue Free Radical Injury

Rubbo

Darley‐Usmar

Freeman

1996

Chem. Res. Toxicol.

271

166

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We have presented evidence from a broad range of chemical, cell biological, and in vivo studies showing that .NO can mediate tissue-protective reactions during oxidant stress, as well as toxic and tissue prooxidant effects. One predominant factor that has been identified which influences .NO being protective versus toxic is the relative rates of production and concentrations of .NO and the more "traditional" family of reactive oxygen species, including O2.-, H2O2, .OH, LO., LOO., and high valency complexes of iron. Also, since so many anti-neutrophil actions of .NO have been described, it is likely that .NO will serve a protective role in acute inflammatory reactions. One issue is certain--many new truths remain to be revealed, as we continue to develop our understanding of the toxicology of reactive oxygen- and nitrogen-containing species.

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Effect of FK409, a Novel Nitric Oxide Donor, on Acute Experimental Myocardial Ischemia

Cited by 22 publications

References 29 publications

Nitric Oxide Donor Sodium Nitroprusside Induces Neurotoxicity in Cerebellar Granular Cell Culture in Rats by an Independent Mechanism from L-Type or Dantrolene-Sensitive Calcium Channels.

Nitric Oxide Donor Sodium Nitroprusside Induces Neurotoxicity in Cerebellar Granular Cell Culture in Rats by an Independent Mechanism from L-Type or Dantrolene-Sensitive Calcium Channels.

Differentiation of the Inhibitory Effects of Calcium Antagonists on Abnormal Behaviors Induced by Methamphetamine or Phencyclidine

Nitric Oxide Regulation of Tissue Free Radical Injury

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