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- Duan, Rui-Dong, et al.
(författare)
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Effects of extracellular calcium and magnesium on bile salt stimulated amylase release from rat pancreatic acini
- 1986
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Ingår i: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 21:10, s. 1211-1216
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Tidskriftsartikel (refereegranskat)abstract
- The effects of extracellular calcium and magnesium on bile-salt-induced amylase release from rat pancreatic acini have been studied. The amylase releases caused by from 0.25 mM to 1.0 mM taurodeoxycholate (TDC) and by taurochenodeoxycholate (TCDC) at a concentration of more than 0.75 mM were reduced by ethylenediaminetetraacetic acid (EDTA) and increased by verapamil. EDTA and verapamil had no significant effect on the taurocholate (TC) (1.0-5.0 mM)-stimulated amylase release. The inhibiting effect of EDTA began to appear already during the initial 5 min and was not parallel to any change of lactate dehydrogenase release. The TDC- and TCDC-stimulated amylase release was strongly dependent on the concentrations of extracellular calcium and was only weakly dependent on extracellular magnesium. The TC-induced amylase release was slightly increased only at high concentrations of calcium and magnesium. It is suggested that the mechanism of dihydroxy bile-salt-induced amylase release from rat pancreatic acini is different from that of trihydroxy bile salt. The dihydroxy bile-salt-stimulated amylase release is dependent on extracellular calcium but does not seem to be related to the uptake of calcium by the acini.
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- Duan, Rui-Dong, et al.
(författare)
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Effects of verapamil on amylase release from rat pancreatic acini and its relation to calcium fluxes.
- 1988
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Ingår i: Pancreas. - : Ovid Technologies (Wolters Kluwer Health). - 0885-3177. ; 3:4, s. 427-432
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Tidskriftsartikel (refereegranskat)abstract
- The effects of verapamil on amylase release and Ca2+ fluxes from rat pancreatic acini have been studied. Verapamil at concentrations above 10 FM dose-dependently inhibited amylase release stimulated by carbachol, but enhanced the amylase release stimulated by cholecystokinin (CCK) and secretin. Verapamil had no significant effect on calcium uptake induced by carbachol or CCK, but significantly inhibited Caf2 eflux caused by carbachol and slightly increased that caused by CCK. In a Ca2+-free, EDTA-containing medium, the increase in cytoplasmic free Ca2+ caused by carbachol was significantly inhibited by verapamil. Verapamil alone up to 400 p, M had no effect on the release of lactic dehydrogenase. In conclusion, the effect of verapamil on amylase release from rat pancreatic acini differs depending on the type of secretagogue used to stimulate amylase release. This effect is not related to blockage of Ca2+ uptake, indicating another mechanism of verapamil on pancreatic acini.
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- Erlanson-Albertsson, Charlotte, et al.
(författare)
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Secretion of pancreatic lipase and colipase from rat pancreas.
- 1987
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Ingår i: Pancreas. - 0885-3177. ; 2, s. 531-535
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Tidskriftsartikel (refereegranskat)abstract
- Rat pancreatic juice was collected from female, anesthetized Sprague-Dawley rats (200–250 g) during basal secretion and after 45-min intravenous infusion for secretin or secretin with cholecystokinin (CCK). The volume of secretion was measured as well as activity of lipase and colipase. It was shown that the basal secretion of pancreatic juice gave a colipase/lipase (C/L) ratio of about 0.5. Stimulation with secretin or addition of CCK to secretin gave a C/L ratio between 0.4 and 0.6. This was not significantly different from the ratio found in basal secretion. The secretion of lipase and colipase from isolated pancreatic acini was also found to parallel a C/L ratio equal to 0.6 in the basal release and to a ratio between 0.5 and 0.6 after stimulation with CCK, secretin, or carbachol. The total activity ratio of C/L in the pancreas was equal to 0.97. It is concluded that lipase and colipase are secreted in parallel both in vivo and in vitro. The reason for a lower ratio of C/L in the secreted juice compared to the C/L ratio of pancreatic gland is not known.
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