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Titolo:
BRADYKININ RECEPTOR SUBTYPES IN RAT LUNG - EFFECT OF INTERLEUKIN-1-BETA
Autore:
TSUKAGOSHI H; HADDAD EB; BARNES PJ; CHUNG KF;
Indirizzi:
NATL HEART & LUNG INST,DEPT THORAC MED,DOVEHOUSE ST LONDON SW3 6LY ENGLAND NATL HEART & LUNG INST,DEPT THORAC MED LONDON SW3 6LY ENGLAND ROYAL BROMPTON HOSP LONDON SW3 6LY ENGLAND
Titolo Testata:
The Journal of pharmacology and experimental therapeutics
fascicolo: 3, volume: 273, anno: 1995,
pagine: 1257 - 1263
SICI:
0022-3565(1995)273:3<1257:BRSIRL>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
GUINEA-PIG; ASTHMATIC SUBJECTS; INHALED BRADYKININ; ANTIGEN CHALLENGE; AIRWAY RESPONSE; SUBSTANCE-P; ANTAGONIST; CELLS; ALLERGEN; PROTEIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
42
Recensione:
Indirizzi per estratti:
Citazione:
H. Tsukagoshi et al., "BRADYKININ RECEPTOR SUBTYPES IN RAT LUNG - EFFECT OF INTERLEUKIN-1-BETA", The Journal of pharmacology and experimental therapeutics, 273(3), 1995, pp. 1257-1263

Abstract

We have characterized bradykinin (BK) receptors in the rat lung and studied the effect of recombinant human interleukin-lp (IL-I beta) on BK receptors in vitro and in vivo. In lung membranes, saturation studies with [(3)]BK revealed a single class of specific and saturable binding sites. The BK B-1 antagonist des-Arg(9)[Leu(8)]-BK was less effective in displacing [H-3]BK binding sites from lung membranes. In contrast, the selective BK B-2 antagonists, Hoe 140 {D-Arg-[Hyp(3),Thi(5),D-Tic(7),Oic(8)]-BK} and NPC 567 {D-Arg-[Hyp(3),D-Phe(7)]-BK} fully inhibited the binding of [H-3]BK to lung membranes with K-i values of 96.7 /- 17.8 pM and 9.0 +/- 2.5 nM, respectively. Intratracheal administration of 500 U of IL-1 beta induced airway hyper-responsiveness to inhaled BK and neutrophilia in bronchoalveolar lavage fluid 18 to 24 hr later. Compared to naive or saline-treated animals, IL-1 beta had no effect on [H-3]BK binding characteristics at 4, 12 or 24 hr after IL-1 beta administration. Twenty-four hours after IL-1 beta instillation, there was no change in the affinity of the selective BK B-1 or B-2 antagonists when compared to control animals. In vivo, the selective BK B-2 receptor antagonists, NPC 567 (3 mu mol kg(-1) i.v.) and Hoe 140 (100 nmol kg(-1) i.v.), inhibited BK-induced increase in lung resistance, whereas the selective BK B-1 antagonist, des-Arg(9)[Leu(8)]-BK (10 mu mol kg(-1) i.v.), was without effect. These data suggest that the action of BK in the rat lung is dependent mainly on the activation of the BK B-2 receptor subtype. Furthermore, the mechanism of IL-1 beta induced airway hyper-responsiveness to BK does not involve the induction of BK B-1 receptors or the up-regulation of BK B-2 receptors in the rat lung.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 00:43:04