Measurement of Endogenous Release of Cholecystokinin by Radioimmunoassay

Reeder, David D.; Becker, H. D.; Smith, Neil; Rayford, Phillip L.; Thompson, James C.

doi:10.1097/00000658-197309000-00010

Cited by 50 publications

(19 citation statements)

References 23 publications

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“…Several earlier studies on concentrations of CCK-like immunoreactivity in human plasma after feeding have suggested concentrations considerably higher (up to 16 ng/ml, or -4 nmol/liter) than those reported here (20)(21)(22). In addition, it has been reported that basal CCK concentrations in celiacs are higher than normal, but postprandial increases are less than normal (23).…”

Section: Discussioncontrasting

confidence: 56%

Identification and measurement of molecular variants of cholecystokinin in duodenal mucosa and plasma. Diminished concentrations in patients with celiac disease.

Calam¹,

Ellis²,

Dockray³

1982

J. Clin. Invest.

151

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A B S T R A C T The amount and type of cholecystokinin (CCK) in duodenal extracts and plasma of celiac patients and normal subjects was studied by radioimmunoassay and gel filtration. In both groups there were similar patterns of molecular forms in extracts of duodenal biopsies, but concentrations in celiac disease were significantly depressed. In boiling water extracts of duodenal mucosa from both groups a factor with the properties of the COOH-terminal octapeptide of cholecystokinin predominated, but there were also significant amounts of a larger molecular weight form. In acid extracts of mucosa a factor with the properties of the 33 or 39 residue form was identified in amounts that were -25% those of CCK8; there were also similar amounts of an acid-soluble form that had an apparent molecular weight higher than CCK39. Plasma immunoreactive cholecystokinin was studied after concentration by immunoaffinity adsorption and fractionation by gel filtration. In normal subjects fasting CCK-like immunoreactivity was <0.8 pmol/liter, and after a light breakfast increased to 2.0±0.7(range 1.0 to 4.8) pmol/liter; CCK8-like activity accounted for all the increased immunoreactivity. In five of six celiac patients the concentrations of both fasting and postprandial CCK-like immunoreactivity in plasma were undetectable (<0.8 pmol/liter). We conclude that diminished production and release of CCK could account for the impaired pancreatic and gall bladder responses to intraluminal stimuli in celiac disease.

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Section: Discussioncontrasting

confidence: 56%

Identification and measurement of molecular variants of cholecystokinin in duodenal mucosa and plasma. Diminished concentrations in patients with celiac disease.

Calam¹,

Ellis²,

Dockray³

1982

J. Clin. Invest.

151

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“…When the glucose was given intraduodenally, the SLI increments from the foregoing sites and in the peripheral venous plasma were smaller, which suggests that unidentified local gastric factors somehow influence gastric and pancreatic SLI (21,22), these gut hormones are candidates for mediators of certain ofthe effects and would also explain, at least in part, the rapidity of the observed changes (23)(24)(25). This possibility is supported by the fact that HC1, which stimulates secretin (25,26) and pancreozymin-cholecystokinin (27) release, elicited prompt increases in SLI release from the pancreas and the antrum, and inferior vena caval SLI levels were approximately doubled. The intraduodenal route of HC1 administration, but not the intragastric route, resulted in a small but significant increase of fundic vein SLI levels.…”

Section: Discussionmentioning

confidence: 96%

Pancreatic and Gastric Somatostatin Release in Response to Intragastric and Intraduodenal Nutrients and HCl in the Dog

Schusdziarra¹,

Harris²,

Conlon³

et al. 1978

J. Clin. Invest.

221

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A B S T R A C T The effects of the instillation of glucose, fat, casein hydrolysate, and HCI into the gastrointestinal tract upon plasma levels of somatostatin-like immunoreactivity (SLI) in the venous effluent of the pancreas, fundus and antrum of the stomach, and in the inferior vena cava (IVC) were determined in normal laparotomized dogs. Fasting SLI levels in the effluent plasma from these sites were significantly greater than IVC levels. The intragastric administration of glucose elicited a prompt and significant rise in SLI levels in pancreatic, fundic and antral venous plasma, and in IVC plasma; intraduodenal glucose elicited smaller increments. After intragastric fat, a smaller, more gradual increase in the pancreatic and fundic effluents was observed, whereas the rise in antral SLI was minute, and IVC SLI did not rise significantly. Intraduodenal fat elicited a prompt increase in the pancreatic and antral vein SLI levels, and a small but significant increase in fundic and IVC plasma which suggests faster release of enteric factors that influence SLI secretion in the pancreas and antrum. Intragastric casein hydrolysate elicited a prompt increase in SLI in both the pancreatic and fundic veins, the latter being marked, but the antral SLI response was small; IVC

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“…Similarly, this increase in response is considered secondary to the vascular smooth muscle relaxing properties which caused the reduction in HAVR. Peripheral serum concentrations of pancreozymin in man have been reported to range between 25-60 pg/ml (Harvey, Dowsett, Hartog & Read, 1973;1974) and as high as 4 ng/ml (Reeder, Becker, Smith, Rayford & Thompson, 1973). These levels rise to between 9 and 17 ng/ml after food containing fats (Harvey et al, 1973;Reeder et al, 1973).…”

Section: Discussionmentioning

confidence: 99%

The Effects of Glucagon, Secretin, Pancreozymin and Pentagastrin on the Hepatic Arterial Vascular Bed of the Dog

Richardson

Withrington

1977

British J Pharmacology

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1The sympathetically-innervated arterial vascular bed of the dog's liver was perfused from a femoral artery. Arterial blood flow and perfusion pressure were monitored continuously and the hepatic arterial vascular resistance (HAVR) calculated from these measurements. 2 Commercial preparations of secretin, pancreozymin, glucagon and pentagastrin were administered by intra-arterial (i.a.) injection and infusion. 3 Secretin and pancreozymin by injection caused dose-dependent hepatic arterial vasodilatation, and on a molar basis were both more potent than glucagon or pentagastrin. 4 Intra-arterial infusions of secretin and pancreozymin caused hepatic arterial vasodilatation at calculated blood concentrations close to those measured under physiological conditions by other investigators. The vasodilatation was of the same duration as that of the hormone infusions. 5Pentagastrin by i.a. injection caused dose-dependent hepatic arterial vasodilatation; by i.a. infusion, vasodilatation occurred but there was marked 'escape' from the effects during the continued infusion.6 As reported previously, glucagon by injection caused dose-dependent hepatic arterial vasodilatation of long duration; by infusion, glucagon caused vasodilatation that persisted after the cessation of the infusion. 7 Glucagon infused i.a., inhibited the vasoconstrictor effects of i.a. noradrenaline, over the same range of infusions that caused hepatic arterial vasodilatation. 8 Secretin or pancreozymin did not antagonize the effects of noradrenaline on the hepatic arterial vascular bed at any doses used. 9 Pentagastrin did not antagonize the vasoconstrictor effect of noradrenaline whether hepatic arterial vasodilatation resulted from the pentagastrin infusion, or not. 10 These results are discussed with respect to the possible control of the hepatic arterial vascular bed by gastrointestinal hormones.

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Measurement of Endogenous Release of Cholecystokinin by Radioimmunoassay

Cited by 50 publications

References 23 publications

Identification and measurement of molecular variants of cholecystokinin in duodenal mucosa and plasma. Diminished concentrations in patients with celiac disease.

Identification and measurement of molecular variants of cholecystokinin in duodenal mucosa and plasma. Diminished concentrations in patients with celiac disease.

Pancreatic and Gastric Somatostatin Release in Response to Intragastric and Intraduodenal Nutrients and HCl in the Dog

The Effects of Glucagon, Secretin, Pancreozymin and Pentagastrin on the Hepatic Arterial Vascular Bed of the Dog

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