cholecystokinin and Hypercalcemia

Topics: Achlorhydria; Acute Kidney Injury; Adenoma, Islet Cell; Adult; Cholecystokinin; Dehydration; Diarrhea; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Hypercalcemia; Hypokalemia; Kidney Diseases; Male; Pancreatic Neoplasms; Protein Precursors; Secretin; Syndrome; Zollinger-Ellison Syndrome

Topics: Adult; Bicarbonates; Calcium; Cholecystokinin; Chymotrypsin; Duodenum; Enzyme Induction; Female; Humans; Hypercalcemia; Intestinal Secretions; Lipase; Male; Middle Aged; Pancreas; Pancreatic Juice; Secretin; Trypsin

Recently, we demonstrated that hypercalcemia causes marked stimulation of feline exocrine pancreatic secretion, and that this effect is absent when a large dose of cholecystokinin (CCK) is infused prior to induction of hypercalcemia. To investigate this effect in more detail, anesthetized cats were given calcium i.v. after preadministration of CCK or urecholine (a cholinergic agonist) at specific doses, or of saline as a control. We found that the hypercalcemia-induced stimulation of pancreatic protein secretion was abolished after preadministration of CCK at large doses. After the prestimulus dose was decreased or the calcium dose was increased, however, the pancreatic secretory response to hypercalcemia was preserved. In contrast, the response to a submaximal dose of CCK was unchanged after prestimulation with a large dose of CCK. Similar results were obtained when urecholine instead of CCK was used as prestimulus. These findings indicate that loss of pancreatic responsiveness to hypercalcemia following prestimulation with CCK is dependent on doses of both prestimulus and calcium used, and that it is not specific for prestimulation with CCK but also inducible by cholinergic agonists. They further suggest that this phenomenon is not due to exhaustion of pancreatic secretory capacity, but may reflect decreased sensitivity to the hypercalcemic stimulus instead.

Topics: Animals; Bethanechol Compounds; Cats; Cholecystokinin; Hypercalcemia; Pancreas; Pancreatic Juice; Premedication

To investigate the effects of acute hypercalcemia on exocrine pancreatic secretion, anesthetized cats were given calcium intravenously. Increasing hypercalcemia (3.7-6.3 mmol/L) evoked a dose-dependent increase in enzyme output that was 12 times greater than in normocalcemic controls (p less than 0.001) and was 60% of subsequent maximal stimulation with intravenous cholecystokinin (CCK). The effect of hypercalcemia on enzyme secretion was abolished when CCK was administered 60 min before calcium and at a dose to cause maximal enzyme output. Atropine did not prevent the calcium-induced increase in enzyme secretion. Pancreatic fluid and bicarbonate outputs were not influenced by hypercalcemia during intravenous administration of small amounts of secretin, but were increased by addition of CCK to the secretin infusion. Hypercalcemia did not induce macroscopic or light-microscopic changes in pancreatic morphology. Plasma levels of both CCK and gastrin were increased (p less than 0.01) during hypercalcemia, with and without precalcium administration of CCK; atropine significantly inhibited (p less than 0.05), but did not abolish the calcium-induced releases of both peptides. These data suggest that in the anesthetized cat, acute hypercalcemia induced by intravenous calcium infusion stimulates pancreatic secretion of enzymes, but not fluid and bicarbonate. Acute hypercalcemia also causes release of CCK and, as shown previously, gastrin. The findings suggest that the stimulatory effect of hypercalcemia on pancreatic enzyme secretion is not dependent on intact cholinergic pathways and is probably not exclusively mediated by release of CCK or gastrin.

Topics: Acute Disease; Amylases; Animals; Atropine; Calcium; Cats; Cholecystokinin; Chymotrypsin; Dose-Response Relationship, Drug; Gastrins; Hypercalcemia; Pancreas; Time Factors

Topics: Animals; Bicarbonates; Calcium; Cats; Cell Membrane Permeability; Cholecystokinin; Female; Hypercalcemia; Hyperparathyroidism; Male; Pancreas; Pancreatic Juice; Pancreatitis; Secretin; Stimulation, Chemical

1. The kinetics of Ca++ and enzyme secretion are of corresponding pattern as well at hydrokinetic as at ecbolic stimulation. 2. Physiological respectively pathophysiologically relevant changes of perfusate Ca++ concentrations do not influence pancreatic Ca++ secretion. Extracellular Ca++ concentrations beyond 12 mEq/1 initiate an enzyme independent Ca++ secretion. 3. Hydrokinetic or ecbolic stimulated pancreatic secretion do not distinguish in calcium/protein ratio. 4. Basal and stimulated enzyme secretion of isolated perfused canine pancreas remain unaffected by increments of extracellular Ca++ concentrations even at pharmacological values. 5. The stimulated enzyme- and Ca++ secretion remain constant during hypocalcemic perfusate conditions but decrease to basal values in Ca++ free media, rapidly and completely reversible by recalcification of the perfusate. 6. The secretin stimulated volume secretion remains unchanged either by extremely hypercalcemic or Ca++ depleted perfusate conditions.

Topics: Animals; Calcium; Cholecystokinin; Dogs; Enzymes; Hypercalcemia; In Vitro Techniques; Pancreas; Pancreatic Juice; Perfusion; Secretin

Hypercalcemia produced in normal volunteers by intravenous infusions of CaCl2 increased outputs of pancreatic enzyme and gastric acid. Further, hypercalcemia enhanced cholecystokinin (CCK)-stimulated pancreatic enzyme secretion and gallbladder contraction. Our results suggest that hypercalcemia affects pancreatic, gallbladder, and gastric functions as well as their responses to exogenous CCK.

Topics: Adult; Bilirubin; Cholecystokinin; Gallbladder; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hypercalcemia; Male; Pancreas; Pancreatic Juice; Stomach

To determine the effect of intraduodenal calcium on pancreatic, gallbladder, and gastric functions in healthy man, a validated perfusion method was employed to quantify total pancreatic, biliary, and gastric outputs during duodenal perfusion of either 6 mM, 12 mM,or 25 mM of elemental calcium (as isotonic calcium chloride solutions). Intraluminal calcium stimulated pancreatic enzyme secretion and gallbladder contraction in a dose-related fashion, achieving comparable responses to those produced by intravenous cholecystokinin-pancreozymin (CCK-z). Responses to calcium were reproducible when repeated in the same individual. Gastric acid outputs and serum gastrin levels increased significantly only with higher calcium perfusions (25 mM). Although duodenal calcium perfusion (25 mM) slightly increased serum calcium concentrations, induced hypercalcemia (by intravenous calcium infusion) of similar magnitude had no effect on pancreatic or gallbladder function. It is suggested that intraduodenal calcium may induce release of CCK-PZ (and/or other neurohormonal factors) from the gut, causing stimulation of these digestive organs.

Topics: Adult; Calcium; Cholecystokinin; Duodenum; Gallbladder; Gastric Juice; Gastrins; Humans; Hypercalcemia; Infusions, Parenteral; Male; Pancreas; Perfusion; Stomach; Trypsin

Topics: Animals; Calcitonin; Calcium; Cholecystokinin; Edetic Acid; Female; Gastric Mucosa; Hypercalcemia; Hypocalcemia; Pancreas; Rats; Secretin; Stimulation, Chemical; Time Factors; Trypsin

Topics: Acute Disease; Adult; Amylases; Bicarbonates; Calcitonin; Cholecystokinin; Female; Humans; Hypercalcemia; Hypocalcemia; Male; Middle Aged; Pancreas; Secretin; Trypsin

Topics: Animals; Calcium; Cats; Cholecystokinin; Chymotrypsin; Duodenum; Humans; Hypercalcemia; Intestinal Secretions; Lipase; Pancreas; Trypsin