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Titolo:
THE ACTIVATION OF NITRIC-OXIDE SYNTHASE BY COPPER-ION IS MEDIATED BY INTRACELLULAR CA2-CELLS( MOBILIZATION IN HUMAN PULMONARY ARTERIAL ENDOTHELIAL)
Autore:
DEMURA Y; ISHIZAKI T; AMESHIMA S; OKAMURA S; HAYASHI T; MATSUKAWA S; MIYAMORI I;
Indirizzi:
FUKUI MED UNIV,DEPT INTERNAL MED 3 MATSUOKA FUKUI 91011 JAPAN FUKUI MED UNIV,CENT RES LABS MATSUOKA FUKUI 91011 JAPAN
Titolo Testata:
British Journal of Pharmacology
fascicolo: 6, volume: 125, anno: 1998,
pagine: 1180 - 1187
SICI:
0007-1188(1998)125:6<1180:TAONSB>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
SMOOTH-MUSCLE CELLS; RELAXING FACTOR; CALCIUM; RELEASE; SUPEROXIDE; HYPERTENSION; RELAXATION; DEFICIENCY; STIMULATE; BREAKDOWN;
Keywords:
COPPER; NITRIC OXIDE; NITRIC OXIDE SYNTHASE; CALCIUM MOBILIZATION; ENDOTHELIAL CELL; DIHYDROPYRIDINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
37
Recensione:
Indirizzi per estratti:
Citazione:
Y. Demura et al., "THE ACTIVATION OF NITRIC-OXIDE SYNTHASE BY COPPER-ION IS MEDIATED BY INTRACELLULAR CA2-CELLS( MOBILIZATION IN HUMAN PULMONARY ARTERIAL ENDOTHELIAL)", British Journal of Pharmacology, 125(6), 1998, pp. 1180-1187

Abstract

1 The aim of the study was to elucidate the vasodilatory mechanism due to Cu2+ by assessing nitric oxide (NO) production as determined by NOx (NO, NO2-, and NO3-) that is released from human pulmonary arterialendothelial cell (HPAEC) monolayers using a NO chemiluminescence analyzer, and also to assess Ca2+ movement using Ca-45 and fura 2 in HPAEC. 2 Cu2+ (10(-6)-10(-4) M) significantly increased NO production in a dose-dependent manner when extracellular Ca2+ was present. 3 Ca-45 influx into the adherent cells was dose-dependently enhanced by Cu2+ (10(-6)-10(-4) M), but not by Mn2+, Zn2+ or Fe2+. 4 [Ca2+](i), measured bymonitoring the fluorescence changes of fura 2, was significantly elevated in the presence of Cu2+. 5 The increase in [Ca2+](i) induced by Cu2+ was inhibited by either diethyldithiocarbamate (DDC) or the depletion of extracellular Ca2+. 6 The dihydropyridine receptor agonist; BayK8644, significantly attenuated the Cu2+-induced increase in [Ca2+](i)in a dose dependent manner and nitrendipine or nifedipine, the dihydropyridine receptor antagonists, dose-dependently inhibited a Cu2+-induced increase in [Ca2+](i). 7 These results suggest that Cu2+ activateseNOS through the mechanism of [Ca2+](i) elevation due to Ca2+ influx-into HPAEC and that the Cu2+-induced [Ca2+](i) elevation in HPAEC is likely due to activation of the dihydropyridine,like receptors.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 10:32:08