G. Le Drean et al., Exogenous CCH and gastrin stimulate pancreatic exocrine secretion via CCK-A but also via CCK-B/gastrin receptors in the calf, PFLUG ARCH, 438(1), 1999, pp. 86-93
A predominance of the pancreatic cholecystokinin (CCK) receptor of the B/ga
strin subtype (CCK-B/G) was reported in calves older than 1 month. Specific
CCK-A and CCK-B/G receptor antagonists (SR 27897 and PD 135158, respective
ly) were used to identify the CCK receptor subtype involved in exogenous CC
K- and gastrin-induced exocrine pancreatic responses. Conscious calves (2 m
onths old) with catheterized pancreas, jugular vein and duodenum were used:
the pancreatic juice was continuously reinfused. CCK (30 pmol kg(-1) min(-
1), 40 min) evoked an increase in pancreatic juice flow and enzyme secretio
n, while the same dose of gastrin increased enzyme secretion alone. CCK-ind
uced pancreatic secretion was abolished by SR 27897 (15 nmol kg(-1) min(-1)
, 55 min) and reduced by PD 135158 (0.15 nmol kg(-1) min(-1), 55 min). Gast
rin-induced enzyme secretion was reduced by PD 135158 (50% to 90%) and to a
lesser extent by SR 27897 (50% to 60%). These results demonstrate that CCK
and gastrin in the physiological range stimulate pancreatic exocrine secre
tion in calves and that these effects are partly mediated by CCK-B/G recept
ors. Although CCK-A receptors are not predominantly expressed, they seem to
play a major role in the response of pancreatic exocrine secretion to CCK.