The effect of cholecystokinin‐related peptides on periodic pancreatic secretion in fasting dogs.

Abstract

1. The effect of cholecystokinin octapeptide (CCK‐8) and pentagastrin on periodic pancreatic secretion was studied in fasting conscious dogs. 2. Both CCK‐8 and pentagastrin, in small doses, prolonged the interval of periodic pancreatic secretion. Periodicity was disrupted by large doses of CCK‐8 and pentagastrin. 3. CCK‐8, at the dose which did not disrupt the cycle, raised the peak and the valley‐to‐valley means, but not the valley mean, of protein secretion in one cycle. Except at large doses, pentagastrin failed to increase the peak and valley mean, but increased mean, valley‐to‐valley protein secretion. Large doses of both pentagastrin and CCK‐8 increased protein secretion at the valley. 4. The peak of periodic pancreatic protein secretion was about half the observed maximum protein response to CCK‐8. 5. Atropine reduced pancreatic fluid and protein responses to small doses of CCK‐8 to the levels of valleys. At large doses, however, both responses were augmented by atropine. Hexamethonium reduced the responses to any dose of CCK‐8 to valley levels or less. Volume and protein responses to pentagastrin following atropine or hexamethonium were of similar magnitude to those at valleys. 6. It is concluded that CCK‐8 and pentagastrin stimulate pancreatic enzyme secretion directly by acting on acinar cells and indirectly by modifying cholinergic ganglionic activities which control periodic secretion in conscious dogs.

Local versus peripheral blood administration of cholecystokinin‐8 and secretin on pancreatic secretion in calves

“…In contrast to intra-arterial infusion, CCK-8 and secretin given intravenously were distributed throughout the circulation, and thus might reach the pancreas directly and stimulate acinar and ductal cells (Milutinovic et al 1976;Van Dijk et al 1984). The CCK-8 and secretin reaching the pancreas might stimulate exocrine pancreatic secretion via release of islet hormones (Saito, Williams & Kanno, 1980;Ahren, Martensson & Nobin, 1988) or modify activity of intra-pancreatic cholinergic ganglia (Magee & Naruse, 1988). Surprisingly low concentrations of CCK and secretin in peripheral blood plasma after local infusion compared with the concentrations after peripheral infusion were not due to the effect of catheter malfunction, since pancreatic secretion was apparently stimulated.…”

Aquaporins in rat pancreatic interlobular ducts

“…In dogs, most of the water (ϳ90%) in the pancreatic juice was derived from the duct. Fluid secretion associated with maximal enzyme secretion from acini by cholecystokinin (CCK) was only 10% of the maximal response to secretin in dogs, in which secretin did not stimulate enzyme secretion (22,23). In rats, fluid originating from these ducts is more difficult to estimate, because both secretin and CCK stimulate fluid and enzyme secretion.…”

Cholecystokinin‐8 and vasoactive intestinal polypeptide stimulate exocrine pancreatic secretion via duodenally mediated mechanisms in the conscious pig

“…Under basal conditions (i.e. following an overnight fast) there are cyclic oscillations in the volume, and the protein and enzyme secretion rate of pancreatic juice (Magee & Naruse, 1988;Zabielski, Onaga, Mineo & Kato, 1993). Moreover, the pancreas may be differently affected by a secretagogue depending on the time of administration during the cycle (Zabielski et al 1993).…”