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Titolo:
Protective role of nitric oxide synthase against ischemia-reperfusion injury in guinea pig myocardial mitochondria
Autore:
Hotta, Y; Otsuka-Murakami, H; Fujita, M; Nakagawa, J; Yajima, M; Liu, W; Ishikawa, N; Kawai, N; Masumizu, T; Kohno, M;
Indirizzi:
Aichi Med Univ, Dept Pharmacol, Aichi 4801195, Japan Aichi Med Univ Aichi Japan 4801195 Dept Pharmacol, Aichi 4801195, Japan Aichi Med Univ, Dept Anat, Aichi 4801195, Japan Aichi Med Univ Aichi Japan 4801195 Univ, Dept Anat, Aichi 4801195, Japan Jeol Ltd, Applicat & Res Ctr, ESR Applicat Lab, Tokyo 1960021, Japan Jeol Ltd Tokyo Japan 1960021 Ctr, ESR Applicat Lab, Tokyo 1960021, Japan
Titolo Testata:
EUROPEAN JOURNAL OF PHARMACOLOGY
fascicolo: 1, volume: 380, anno: 1999,
pagine: 37 - 48
SICI:
0014-2999(19990903)380:1<37:PRONOS>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
NUCLEAR-MAGNETIC-RESONANCE; RAT-LIVER MITOCHONDRIA; L-ARGININE; OXYGEN RADICALS; INFARCT SIZE; HEART; SUPEROXIDE; CA2+; DIHYDROOUABAIN; DYSFUNCTION;
Keywords:
myocardial mitochondria; ischemia-reperfusion injury; nitric oxide (NO center dot); endothelial nitric oxide (NO center dot) synthase; reactive oxygen species; EPR (electron paramagnetic resonance) spectrometry; (guinea pig);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Hotta, Y Aichi Med Univ, Dept Pharmacol, 21 Yazakoaza Karimata Nagakute, Aichi 4801195, Japan Aichi Med Univ 21 Yazakoaza Karimata Nagakute Aichi Japan 4801195
Citazione:
Y. Hotta et al., "Protective role of nitric oxide synthase against ischemia-reperfusion injury in guinea pig myocardial mitochondria", EUR J PHARM, 380(1), 1999, pp. 37-48

Abstract

In guinea-pig myocardial mitochondria preparation, lowering the Ca2+ concentration or pH level in the perfusate rapidly elevated the fura-2 Ca2+ signal ([Ca2+](m)). Pretreatment with 10(-4) M L-Arg inhibited the rapid [Ca2+](m) influx, whereas administration of 10(-4) M L-NAME did not, suggesting some association between nitric oxide (NO .) synthase (NOS) activation and Ca2+ kinetics in mitochondria. Immunoblotting analysis showed that endothelial (e)-NOS was present in mitochondria, but not inducible (i)-NOS or brain (b)-NOS. Electron microscopy observations revealed that the e-NOS antibody-reactive site in the mitochondria was the inner cristae. The production of reactive oxygen species and NO . in isolated mitochondria was detected by the spin trapping technique with electron paramagnetic resonance (EPR) spectrometry. Pretreatment with 10(-5) M S-nitroso-N-acetyl-DL-penicillamine (SNAP) and 10(-5) M 3-[2-Hydroxy-1-(1-methylethyl)-2-nitrosohydrazino]-1-propanaine (NOC 5), which spontaneously generate NO ., completely inhibited the [Ca2+](m) uptake. In addition, N-morpholino sydnonimine hydrochloride (SIN-1) (10(-5) M), which simultaneously generates NO as well as . O-2(-) and peroxynitrite anion (ONOO-), inhibited the increase in [Ca2+](m). ONOO- (3 X 10(-4) M) itself also inhibited this increase. Pretreatment with the . O-2(-)-scavenger manganese superoxide dismutase or catalase (200 units/ml) completely inhibited the increase in [Ca2+](m) caused by lowering of either theCa2+ concentration or the pH in the perfusate. These results suggested that the formation of reactive oxygen species promoted the [Ca2+](m) influx. The agents that inhibited the [Ca2+](m) influx improved contractility even in Langendorff preparations after ischemia. Based on these findings, we concluded that e-NOS exists in mitochondria and that NO . may play an importantprotective role in reperfusion cardiac injury after ischemia, by inhibiting the Ca2+ influx into mitochondria which are otherwise damaged by . O-2(-). (C) 1999 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 23:50:04