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Titolo:
LINKAGE OF [CA2-CELLS TO SOMATOSTATIN SECRETION INDUCED BY CHOLECYSTOKININ(](I) IN SINGLE ISOLATED D)
Autore:
DELVALLE J; WAKASUGI J; TAKEDA H; YAMADA T;
Indirizzi:
UNIV MICHIGAN,MED CTR,DEPT INTERNAL MED,6520 MSEBI ANN ARBOR MI 48109 UNIV MICHIGAN,MED CTR,DEPT PHYSIOL ANN ARBOR MI 48109
Titolo Testata:
American journal of physiology: Gastrointestinal and liver physiology
fascicolo: 6, volume: 33, anno: 1996,
pagine: 897 - 901
SICI:
0193-1857(1996)33:6<897:LO[TSS>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
FUNDIC MUCOSAL CELLS; CANINE; IMMUNOREACTIVITY; OSCILLATIONS; CULTURE;
Keywords:
GUT PEPTIDES; CALCIUM CHANNELS; SIGNAL TRANSDUCTION; NIFEDIPINE; L-364,718; INTRACELLULAR CALCIUM CONCENTRATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
15
Recensione:
Indirizzi per estratti:
Citazione:
J. Delvalle et al., "LINKAGE OF [CA2-CELLS TO SOMATOSTATIN SECRETION INDUCED BY CHOLECYSTOKININ(](I) IN SINGLE ISOLATED D)", American journal of physiology: Gastrointestinal and liver physiology, 33(6), 1996, pp. 897-901

Abstract

The Ca2+/inositol phospholipid signaling cascade has been implicated in the mechanism by which cholecystokinin (CCK) stimulates gastric somatostatin release, but a direct linkage between intracellular events in gastric D cells and somatostatin secretion has not been established. To address this problem we developed a method for correlating somatostatin release with the measurement of intracellular Ca2+ concentration([Ca2+](i)) in isolated D cells. Resting [Ca2+](i) in single D cells was 100 +/- 5.7 nM (means +/- SE, n = 41), and CCK induced a rise in [Ca2+](i) in a dose-dependent fashion, producing a maximal stimulatory effect (243 +/- 15% of control, n = 12) at a peptide concentration of 2 x 10(-8) M. The CCK-mediated increase in [Ca2+](i) was biphasic, with a rapid, initial transient elevation followed by a sustained plateau. The rise in [Ca2+](i) was accompanied by a concomitant increase in release of somatostatin-like immunoreactivity (SLI). Removal of extracellular Ca2+ had no effect on the initial transient elevation in [Ca2+](i) induced by CCK but abolished both the sustained plateau in [Ca2+](i) and the release of SLI. The selective CCK antagonist L-364,718 (10(-7) M) inhibited the effects of CCK on both [Ca2+](i) and SLI release. The nonspecific Ca2+ channel blocker NiCl2 (10(-3) M) and the L-type Ca2+ channel blocker nifedipine inhibited the sustained rise in [Ca2+](i) and the release of SLI but left the initial transient increase in [Ca2+](i) unaltered. These results indicate that CCK-stimulated release of SLI from D cells in the gastric fundus is linked to influx of extracellular Ca2+ via L-type Ca2+ channels.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 17:02:40