Role of cholecystokinin in intestinal phase of human pancreatic secretion

Abstract

In this study we have utilized a sensitive and specific radioimmunoassay for cholecystokinin (CCK) to determine the effects of a jejunal infusion (5 cc/min) of amino acids (44 g/liter), saline, and amino acids with intravenous atropine (20 micrograms X lg-1 X hr) on pancreatic exocrine secretion. Amino acids were found to stimulate pancreatic output of trypsin and release CCK, while a saline infusion at the same rate and osmolality (320 mosm/liter) failed to do so. In the presence of atropine, the amino acid infusion did not stimulate the pancreatic output of trypsin, despite an augmented CCK release. The total CCK released above baseline was greatest with the infusion of amino acids with atropine, while the total trypsin output above baseline was greatest with the infusion of amino acids. These results indicate that CCK release is not under cholinergic control and that cholinergic blockade inhibits pancreatic secretion by interrupting stimulating cholinergic fibers to the pancreas.

Effect of Atropine on Intestinal Phase of Pancreatic Secretion in Man

“…These results confirm earlier findings on the failure of atropine to alter plasma CCK lev els under basal conditions and after endoge nous stimulation by either com oil or amino acids [4,8], Thus, enteropancreatic reflexes exist which mediate pancreatic enzyme se cretion without interfering with CCK re lease. In the present study, the cholinergic control was surpassed from 10 to 30 min after meal stimulation by endogenous re lease of CCK.…”

“…In recent studies, atropine did not inhibit the stimulated CCK response to intraduodenal fat or amino acids, but almost completely suppressed the stimulation of en zyme secretion [4,8,20]. These results sup port the concept of a cholinergic, enteropancreatic reflex as it was convincingly demon strated in the dog by Singer et al [16,17] and Solomon and Grossman [18].…”

“…This could result from duo denal distension by the test meal and the high offer of peptides and fatty acids at the site of CCK-producing cells. Intraduodenal infusions of small amounts of saline do not cause an increase in plasma CCK levels [4,19]. However, there is ample evidence that duodenal volume receptors and osmorecep tors exist in man, which regulate pancreatic secretion via cholinergic reflexes [5,13].…”

“…The inges tion of a meal or of food constituents like fat or amino acids causes an increase in plasma concentrations of cholecystokinin (CCK) and secretin [1,4,8]. When the CCK ana logue caerulein is infused in concentrations which reach postprandial plasma levels of CCK, the pancreatic secretory response is similar to that found after a meal [1],…”

Cholecystokinin release and biliopancreatic secretion in response to selective perfusion of the duodenal loop with aminoacids in man.

“…Selective duodenal infusion (10 mi/min) of AA1 induced a frank increase in bile salt output (Fig. 2) but a small and non-significant augmentation of lipase and chymotrypsin secretion: 2.12 (0.44) kU/min v 153 (0.6) and 141 (35) U/min v 119 (18) respectively. There was concomitantly a sharp increase in plasma CCK concertrations (Fig.…”