Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Involvement of CYP3A-derived arachidonic acid metabolite(s) in responses to endothelium-derived KC channel opening substance in monkey lingual artery
Autore:
Ayajiki, K; Okamura, T; Fujioka, H; Imaoka, S; Funae, Y; Toda, N;
Indirizzi:
Shiga Univ Med Sci, Dept Pharmacol, Ohtsu, Shiga 5202192, Japan Shiga UnivMed Sci Ohtsu Shiga Japan 5202192 Ohtsu, Shiga 5202192, Japan Osaka City Univ, Sch Med, Dept Biol Chem, Osaka 5458585, Japan Osaka City Univ Osaka Japan 5458585 Dept Biol Chem, Osaka 5458585, Japan
Titolo Testata:
BRITISH JOURNAL OF PHARMACOLOGY
fascicolo: 3, volume: 128, anno: 1999,
pagine: 802 - 808
SICI:
0007-1188(199910)128:3<802:IOCAAM>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT POTASSIUM CHANNELS; EDHF-MEDIATED RELAXATION; RAT HEPATIC-ARTERY; EPOXYEICOSATRIENOIC ACIDS; HYPERPOLARIZING FACTOR; CYTOCHROME-P450 3A4; CAROTID-ARTERY; NITRIC-OXIDE; MICROSOMES; ANANDAMIDE;
Keywords:
cytochrome P450 mono-oxygenase; K+ channel; endothelium-dependent relaxation; lingual artery; acetylcholine;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Toda, N Shiga Univ Med Sci, Dept Pharmacol, Ohtsu, Shiga 5202192, Japan Shiga Univ Med Sci Ohtsu Shiga Japan 5202192 Shiga 5202192, Japan
Citazione:
K. Ayajiki et al., "Involvement of CYP3A-derived arachidonic acid metabolite(s) in responses to endothelium-derived KC channel opening substance in monkey lingual artery", BR J PHARM, 128(3), 1999, pp. 802-808

Abstract

1 In monkey lingual artery strips partially contracted with prostaglandin F-2/x, acetylcholine-induced, concentration-related relaxations were abolished by removal of the endothelium. The response was not significantly influenced by indomethacin but attenuated by N-G-nitro-L-arginine (L-NOARG); theeffect of the nitric oxide (Na) synthase inhibitor was reversed by L-arginine.2 The response to acetylcholine resistant to L-NOARG was suppressed in thestrips exposed to high K+ media. Charybdotoxin partially inhibited the relaxation, and the remaining relaxation was abolished by additional treatmentwith apamin, whereas glibenclamide, iberiotoxin or apamin alone was without effect. Relaxations induced by sodium nitroprusside were not influenced by charybdotoxin.3 The L-NOARG-resistant acetylcholine-induced relaxation was inhibited by metyrapone, proadifen and 17-octadecynoic acid, non-selective cytochrome P450 mono-oxygenase (CYP) inhibitors, and progesterone and ketoconazole, inhibitors selective to CYP3A. The inhibitors did not affect the nitroprusside-induced relaxation. Selective inhibitors of other CYP isoforms, such as debrisoquine and lauric acid, did not reduce the response to acetylcholine.4 Reaction mixture containing human liver microsome rich in CYPs, arachidonic acid and NADPH incubated at 37 degrees C and filtrated relaxed endothelium-denuded monkey lingual artery strips, used as bioassay tissues. This response was abolished in the strips exposed to high K+ media. The response was also suppressed by combined treatment of the assay tissue with charybdotoxin plus apamin, but was not affected by treatment with iberiotoxin. The reaction mixture co-incubated with ketoconazole failed to relax the strips.5 It is concluded that the monkey lingual arterial relaxation dependent onthe endothelium is mediated by NO and also by a charybdotoxin plus apamin-sensitive but iberiotoxin-insensitive Ca2+-activated K+ channel opening substance(s) that may be a CYP3A-derived arachidonic acid metabolite(s).

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/01/20 alle ore 15:36:22