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Titolo:
Modulation of ET-1-induced contraction of human bronchi by airway epithelium-dependent nitric oxide release via ETA receptor activation
Autore:
Naline, E; Bertrand, C; Biyah, K; Fujitani, Y; Okada, T; Bisson, A; Advenier, C;
Indirizzi:
Fac Med Paris Ouest, Pharmacol Lab, F-75270 Paris, France Fac Med Paris Ouest Paris France F-75270 acol Lab, F-75270 Paris, France Ctr Hosp Versailles, F-78150 Le Chesnay, France Ctr Hosp Versailles Le Chesnay France F-78150 F-78150 Le Chesnay, France Ciba Geigy AG, Resp Dis & Allergy Dept, CH-4002 Basel, Switzerland Ciba Geigy AG Basel Switzerland CH-4002 Dept, CH-4002 Basel, Switzerland Ciba Geigy Japan Ltd, Int Res Labs, Takarazuka, Hyogo 665, Japan Ciba Geigy Japan Ltd Takarazuka Hyogo Japan 665 arazuka, Hyogo 665, Japan Ctr Medicochirurg Val dOr, F-92210 St Cloud, France Ctr Medicochirurg Val dOr St Cloud France F-92210 92210 St Cloud, France
Titolo Testata:
BRITISH JOURNAL OF PHARMACOLOGY
fascicolo: 2, volume: 126, anno: 1999,
pagine: 529 - 535
SICI:
0007-1188(199901)126:2<529:MOECOH>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
GUINEA-PIG TRACHEA; ET(B) RECEPTOR; SMOOTH-MUSCLE; ENDOTHELIN RECEPTORS; 3 ENDOTHELINS; HIGHLY POTENT; CELLS; ANTAGONISTS; ET(A); RELAXATION;
Keywords:
endothelin-1; human bronchus; ETA receptors; ETB receptors; IRL 1620; BQ-123; BQ-788; nitric oxide; airway epithelium;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Naline, E Lab Pharmacol Resp, 15 Rue Ecole Med, F-75006 Paris, France Lab Pharmacol Resp 15 Rue Ecole Med Paris France F-75006 France
Citazione:
E. Naline et al., "Modulation of ET-1-induced contraction of human bronchi by airway epithelium-dependent nitric oxide release via ETA receptor activation", BR J PHARM, 126(2), 1999, pp. 529-535

Abstract

1 The purpose of this work was to investigate whether endothelin-1 (ET-1) was able to induce the release of an inhibitory factor from the airway epithelium in isolated human bronchi and to identify this mediator as well as the endothelin receptor involved in this phenomenon.2 In intact bronchi, ET-1 induced a concentration-dependent contraction (-logEC(50) = 7.92 +/- 0.09, n = 18) which was potentiated by epithelium removal (-logEC(50) = 8.65 +/- 0.11, n = 17). BQ-123, an ETA receptor antagonist, induced a significant leftward shift of the ET-1 concentration-response curve (CRC). This leftward shift was abolished after epithelium removal.3 L-NAME (3 x 10(-3) M), an inhibitor of nitric oxide (NO) synthase, induced a significant leftward shift of the ET-1 CRC, and abolished the potentiation by BQ-123 (10(-8) M) of ET-1-induced contraction.4 In intact preparations, the ETB receptor antagonist BQ-788 induced only at 10(-5) M a slight rightward shift of the ET-1 CRC. In contrast, in epithelium-denuded bronchi or in intact preparations in the presence of L-NAME, BQ-788 displayed a non-competitive antagonism toward ET-1-induced contraction.5 IRL 1620, a selective ETB receptor agonist, induced a contraction of theisolated bronchus (-logEC(50) = 7.94 +/- 0.11, n = 19). This effect was not modified by epithelium removal or by BQ-123. BQ-788 exerted a competitiveantagonism against IRL 1620 which was similar in the presence or absence of epithelium.6 These results show that ET-1 exerts two opposite effects on the human airway smooth muscle. One is contractile via ETB-receptor activation, the other is inhibitory and responsible of NO release which counteracts via ETA-receptor activation the contraction.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 14/07/20 alle ore 08:52:49