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Titolo:
SOMATOSTATIN INHIBITS GASTRIN-RELEASE AND ACID-SECRETION BY ACTIVATING SST(2) IN DOGS
Autore:
LLOYD KCK; AMIRMOAZZAMI S; FRIEDIK F; CHEW P; WALSH JH;
Indirizzi:
UNIV CALIF DAVIS,SCH VET MED,DEPT ANAT PHYSIOL & CELL BIOL DAVIS CA 95616 W LOS ANGELES VET AFFAIRS MED CTR,RES SERV LOS ANGELES CA 90073 W LOS ANGELES VET AFFAIRS MED CTR,MED SERV LOS ANGELES CA 90073 W LOS ANGELES VET AFFAIRS MED CTR,CURE,DIGEST DIS RES CTR LOS ANGELESCA 90073 UNIV CALIF LOS ANGELES,SCH MED,DEPT MED LOS ANGELES CA 90095 UNIV CALIF LOS ANGELES,SCH MED,DEPT PHYSIOL LOS ANGELES CA 90095
Titolo Testata:
American journal of physiology: Gastrointestinal and liver physiology
fascicolo: 6, volume: 35, anno: 1997,
pagine: 1481 - 1488
SICI:
0193-1857(1997)35:6<1481:SIGAAB>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
FAT-INDUCED INHIBITION; PERFUSED RAT STOMACH; MONOCLONAL-ANTIBODY IMMUNONEUTRALIZATION; ENTEROCHROMAFFIN-LIKE CELLS; HISTAMINE-RELEASE; PRIMARY CULTURE; INTESTINAL FAT; RECEPTOR SUBTYPE; PARIETAL-CELLS; MUCOSAL CELLS;
Keywords:
SOMATOSTATIN RECEPTORS; STOMACH; G CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
55
Recensione:
Indirizzi per estratti:
Citazione:
K.C.K. Lloyd et al., "SOMATOSTATIN INHIBITS GASTRIN-RELEASE AND ACID-SECRETION BY ACTIVATING SST(2) IN DOGS", American journal of physiology: Gastrointestinal and liver physiology, 35(6), 1997, pp. 1481-1488

Abstract

Somatostatin is a potent inhibitor of gastrin-stimulated acid secretion by activation of somatostatin receptor type 2 (sst(2)) in vivo, probably in part by blocking gastrin-stimulated histamine release from enterochromaffin-like cells expressing sst(2). We propose that activation of sst(2) may also regulate meal-stimulated acid secretion by blocking gastrin release from antral G cells. Using peptide analogs relatively selective for sst(2) (NC-8-12), sst(3) (BIM-23058), and sst(5) (BIM-23052), we tested this hypothesis in two ways: first, in vivo by measuring plasma gastrin release during meal-stimulated acid secretion in dogs, and second, in vitro by measuring bombesin-stimulated gastrin release from an enriched culture of canine antral G cells. In vivo, a low dose (0.05 nmol.kg(-1).h(-1)) of NC-8-12 inhibited acid secretion 56+/- 16% without blocking gastrin release. A higher dose (1 nmol.kg(-1).h(-1)) of NC-8-12 abolished acid secretion and inhibited gastrin release by 61 +/- 4%, whereas the highest dose (5 nmol.kg(-1).h(-1)) inhibited gastrin release by 84 +/- 3%. Only the highest doses (5 nmol.kg(-1).h(-1)) of BIM-23058 and BIM-23052 significantly inhibited gastrin release and acid secretion. In vitro, NC-8-12 (10(-9) M) reduced bombesin-stimulated gastrin release from antral G cells by 49 +/- 5%, whereas BIM-23058 and BIM-23052 were at least 100-fold less effective. These results indicate that somatostatin activation of sst(2), but not sst(3) Or sst(5), is the major pathway for somatostatin-induced inhibition of meal-stimulated gastrin release and acid secretion.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 15:33:18