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Titolo:
VASOPRESSIN INDUCES FREQUENCY-MODULATED REPETITIVE CALCIUM TRANSIENTSIN SINGLE INSULIN-SECRETING HIT CELLS
Autore:
SCHOFL C; SCHULTE P; ROSSIG L; VONZURMUHLEN A; BRABANT G;
Indirizzi:
HANNOVER MED SCH,KLIN ENDOKRINOL ABT D-30623 HANNOVER GERMANY
Titolo Testata:
Molecular and cellular endocrinology
fascicolo: 1-2, volume: 108, anno: 1995,
pagine: 185 - 192
SICI:
0303-7207(1995)108:1-2<185:VIFRCT>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
PANCREATIC BETA-CELLS; PROTEIN-KINASE-C; PAROTID ACINAR-CELLS; ARGININE-VASOPRESSIN; INOSITOL PHOSPHATE; CYTOSOLIC CA-2+; RAT PANCREAS; GLUCOSE; LINE; RELEASE;
Keywords:
ARGININE-VASOPRESSIN; INTRACELLULAR FREE CA2+; CA2+ TRANSIENTS; VOLTAGE-DEPENDENT CA2+ CHANNELS; THAPSIGARGIN; INSULIN SECRETION; HIT CELL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
39
Recensione:
Indirizzi per estratti:
Citazione:
C. Schofl et al., "VASOPRESSIN INDUCES FREQUENCY-MODULATED REPETITIVE CALCIUM TRANSIENTSIN SINGLE INSULIN-SECRETING HIT CELLS", Molecular and cellular endocrinology, 108(1-2), 1995, pp. 185-192

Abstract

Ca2+ is central to the stimulation of insulin secretion from pancreatic beta-cells. Arginine-vasopressin (AVP) may participate in the modulation of insulin release. In the present study, the AVP-induced changes in cytosolic free Ca2+ ([Ca2+](i)) were investigated in single fura-2 loaded insulin-secreting HIT cells. Stimulation with AVP (0.1-5 nM) caused repetitive Ca2+ transients. The frequency but not the amplitudeof the Ca2+ transients was modulated by the concentration of AVP. High concentrations of AVP (10-100 nM) triggered a biphasic rise in [Ca2+](i). In Ca2+-free medium AVP caused only one or two Ca2+ transients. Withdrawal of extracellular Ca2+ rapidly abolished the AVP-induced Ca2 transients in all cells tested. The Ca2+ channel blocker, verapamil (50 mu M), reduced amplitude and frequency of the Ca2+ transients by about 25% and 60%, respectively, and terminated the Ca2+ transients in 2 of 6 cells. When HF cells were incubated in Ca2+-free medium, and extracellular Ca2+ was restored, there was a small increase in [Ca2+](i). If, however, the agonist-sensitive Ca2+ pool was functionally depleted by repetitive stimulation with high concentrations of AVP or thapsigargin in Ca2+-free medium before extracellular Ca2+ was restored, an agonist-independent increase in [Ca2+](i) was observed, which was transiently larger than in the control cells, and was mainly preserved in the presence of verapamil. Thus, depletion of the agonist-sensitive Ca2+ pool enhances the influx of extracellular Ca2+ through a Ca2+ entrymechanism independent from verapamil-sensitive voltage-dependent Ca2channels (VDCC). In conclusion, the AVP-induced Ca2+ response in single HIT cells is periodic in nature with frequency-modulated repetitiveCa2+ transients. AVP mobilizes Ca2+ from intracellular pools, but influx of extracellular Ca2+ partly through verapamil-sensitive VDCC, andpartly through an additional, VDCC-independent pathway, which could be controlled by the filling state of the agonist-sensitive Ca2+ pool, is required for maintaining the repetitive nature of the Ca2+ response.

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Documento generato il 05/12/20 alle ore 01:20:02