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Titolo:
REVERSAL BY NPY, PYY AND 3-36-MOLECULAR-FORMS OF NPY AND PYY OF INTRACISTERNAL CRF-INDUCED INHIBITION OF GASTRIC-ACID SECRETION IN RATS
Autore:
GUE M; JUNIEN JL; REEVE JR; RIVIER J; GRANDT D; TACHE Y;
Indirizzi:
W LOS ANGELES VET AFFAIRS MED CTR,CURE,DIGEST DIS RES CTR,DEPT MED,11301 WILSHIRE BLVD LOS ANGELES CA 90073 W LOS ANGELES VET AFFAIRS MED CTR,CURE,DIGEST DIS RES CTR,DEPT MED LOS ANGELES CA 90073 UNIV CALIF LOS ANGELES,BRAIN RES INST LOS ANGELES CA 90073 JOUVEINAL RES INST F-94260 FRESNES FRANCE SALK INST BIOL STUDIES,CLAYTON FDN LABS PEPTIDE BIOL LA JOLLA CA 92037 UNIV ESSEN GESAMTHSCH,DIV GASTROENTEROL ESSEN GERMANY
Titolo Testata:
British Journal of Pharmacology
fascicolo: 2, volume: 118, anno: 1996,
pagine: 237 - 242
SICI:
0007-1188(1996)118:2<237:RBNPA3>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
CORTICOTROPIN-RELEASING FACTOR; NEUROPEPTIDE-Y; SIGMA-RECEPTORS; AUTORADIOGRAPHIC LOCALIZATION; PEPTIDE-YY; BRAIN-STEM; JO-1784; LIGAND; STRESS;
Keywords:
NEUROPEPTIDE Y (NPY); PEPTIDE YY (PYY); SIGMA RECEPTOR; CORTICOTROPIN-RELEASING FACTOR (CRF); GASTRIC ACID SECRETION; CENTRAL NERVOUS SYSTEM; PENTAGASTRIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
38
Recensione:
Indirizzi per estratti:
Citazione:
M. Gue et al., "REVERSAL BY NPY, PYY AND 3-36-MOLECULAR-FORMS OF NPY AND PYY OF INTRACISTERNAL CRF-INDUCED INHIBITION OF GASTRIC-ACID SECRETION IN RATS", British Journal of Pharmacology, 118(2), 1996, pp. 237-242

Abstract

1 The Y receptor subtype involved in the antagonism by neuropeptide Y(NPY) of intracisternal corticotropin-releasing factor (CRF)-induced inhibition of gastric acid secretion was studied in urethane-anaesthetized rats by use of peptides with various selectivity for Y-1, Y-2 andY-3 subtypes: NPY, a Y-1, Y-2 and Y-3 agonist, peptide YY (PYY), a Y-1 and Y-2 agonist, [Leu(31), Pro(34)]-NPY, a Y-1 and Y-3 agonist, NPY(3-36) and PYY(3-36), highly selective Y-2 agonists and NPY(13-36) a weak Y-2 and Y-3 agonist. Peptides were injected intracisternally 10 minbefore intracisternal injection of CRF (10 mu g) and gastric acid secretion was measured by the flushed technique for 1 h before and 2 h after pentagastrin-(10 mu g kg(-1) h(-1), i.v.) infusion which started 10 min after CRF injection. 2 Intracisternal injection of CRF (10 mu g)inhibited by 56% gastric acid secretion stimulated by pentagastrin. Intracisternal injection of NPY and PYY (0.1-0.5 mu g) did not influence the acid response to pentagastrin but blocked CRF-induced inhibitionof pentagastrin-stimulated acid secretion. NPY(3-36) (0.5 mu g) and PYY(3-36) (0.25 and 0.5 mu g) also completely blocked the inhibitory action of CRF on pentagastrin-stimulated acid secretion. 3 [Leu(31), Pro(34)]-NPY (0.5-5 mu g) and NPY(13-36) (0.5-5 mu g) injected intracisternally did not modify gastric acid secretion induced by pentagastrin or CRF inhibitory action. 4 The sigma antagonist, BMY 14802 (1 mg kg(-1) s.c.) did not influence the acid response to pentagastrin but prevented the antagonism by PW(3-36) (0.5 mu g) of the CRF antisecretory effect. 5 These results show that both PYY and NPY and the 3-36 forms of PYY and NPY are equipotent in blocking central CRF-induced inhibition of pentagastrin-stimulated gastric acid secretion. The structure activity profile suggests a mediation through Y-2 receptor subtype and the involvement of sigma binding sites.

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Documento generato il 03/12/20 alle ore 12:53:21