Somatostatin inhibits VIP-stimulated amylase release from perifused guinea pig pancreatic acini

Pomila Singh, I. Asada, A. Owlia, T. J. Collins, J. C. Thompson

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15 Citations (Scopus)

Abstract

We have examined the direct effect of somatostatin (SRIF) on basal and stimulated amylase release from guinea pig pancreatic acini using the in vitro method of continuous perifusion. The optimal conditions of flow rate, chamber size, acinar cell volume per chamber, and period of secretagogue infusion were defined for the perifusion system. The kinetic profile of amylase release in response to cholecystokinin-octapeptide (CCK-8), vasoactive intestinal peptide (VIP), and SRIF was studied. Under optimal conditions, the acini were found to remain equally responsive to an ED50 dose of CCK-8 (0.5-0.8 nM) for 12 h of perifusion. The duration of amylase response to any given dose of CCK-8, given for the optimal period of 5 min, was 80-100 min. The total amylase released minus the basal release divided by 90 min (Δ response) in response to the maximum effective (Max(eff)) dose of CCK-8 (100 nM) was 14,667 ± 1,433 U/l (amounting to a 10-fold increase compared with basal values). When compared with the amount of total Δ amylase released in response to the Max(eff) dose of CCK, the total amylase released in response to the Max(eff) dose of CCK, the total amylase released in response to the Max(eff) doses of SRIF (1 μM) and VIP (10 nM) was 10-21% and 51-59%, respectively. SRIF (100 nM) significantly decreased VIP- (0.1-1.0 nM) stimulated amylase release by 45-70% in the perifusion method of study but had no significant effect on the CCK-stimulated amylase release. This suggests that the perifusion method can be used for investigating the mechanism of SRIF-mediated inhibition of VIP effects on amylase release in an in vitro system.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Volume254
Issue number2
StatePublished - 1988

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Vasoactive Intestinal Peptide
Amylases
Somatostatin
Guinea Pigs
Sincalide
Acinar Cells
Cell Size

ASJC Scopus subject areas

  • Physiology
  • Gastroenterology

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Somatostatin inhibits VIP-stimulated amylase release from perifused guinea pig pancreatic acini. / Singh, Pomila; Asada, I.; Owlia, A.; Collins, T. J.; Thompson, J. C.

In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 254, No. 2, 1988.

Research output: Contribution to journalArticle

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abstract = "We have examined the direct effect of somatostatin (SRIF) on basal and stimulated amylase release from guinea pig pancreatic acini using the in vitro method of continuous perifusion. The optimal conditions of flow rate, chamber size, acinar cell volume per chamber, and period of secretagogue infusion were defined for the perifusion system. The kinetic profile of amylase release in response to cholecystokinin-octapeptide (CCK-8), vasoactive intestinal peptide (VIP), and SRIF was studied. Under optimal conditions, the acini were found to remain equally responsive to an ED50 dose of CCK-8 (0.5-0.8 nM) for 12 h of perifusion. The duration of amylase response to any given dose of CCK-8, given for the optimal period of 5 min, was 80-100 min. The total amylase released minus the basal release divided by 90 min (Δ response) in response to the maximum effective (Max(eff)) dose of CCK-8 (100 nM) was 14,667 ± 1,433 U/l (amounting to a 10-fold increase compared with basal values). When compared with the amount of total Δ amylase released in response to the Max(eff) dose of CCK, the total amylase released in response to the Max(eff) dose of CCK, the total amylase released in response to the Max(eff) doses of SRIF (1 μM) and VIP (10 nM) was 10-21{\%} and 51-59{\%}, respectively. SRIF (100 nM) significantly decreased VIP- (0.1-1.0 nM) stimulated amylase release by 45-70{\%} in the perifusion method of study but had no significant effect on the CCK-stimulated amylase release. This suggests that the perifusion method can be used for investigating the mechanism of SRIF-mediated inhibition of VIP effects on amylase release in an in vitro system.",
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