GTP-Rap1 is involved in evoked pancreatic amylase release.
β-Galactosidase (β-Gal; vector control) and
Rap1GAP-overexpressing acini were stimulated with different concentrations of
either CCK (A), carbachol (B), and cAMP-evoked secretagogues
(C) for 30 min, and amylase release was measured. An inhibition of
amylase secretion (40%) was observed when the Rap1GAP-overexpressing acini
were stimulated with high concentrations of either CCK or carbachol. In
addition, Rap1GAP overexpression decreased 8-Br-cAMP-, CPT-Me-cAMP-, and
VIP-stimulated amylase secretion by 60%. Data shown are means ± S.E.
(4–6 experiments) of amylase release expressed as a percentage of total.
□, β-galactosidase-expressing cells; ▪, Rap1GAP-overexpressing
cells. *, p < 0.05; **, p <
0.01; ***, p < 0.001 versus control; †,
p < 0.05; ††, p < 0.01 versus
CCK, carbachol, 8-Br-cAMP, CPT-Me-cAMP, or VIP response in
β-galactosidase-expressing cells. D, pancreatic acini were
preincubated for 10 min with the PKA inhibitor H-89 and then stimulated with
8-Br-cAMP, CPT-Me-cAMP, or VIP. Secretagogue-stimulated amylase release was
not modified in the presence of the inhibitor. Data shown are means ±
S.E. (four experiments) of amylase release expressed as a percentage of the
total. *, p < 0.05 versus control; †,
p < 0.05 versus 8-Br-cAMP or VIP.