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At least 19 recordsLinked to original sources
PubMed1978

The choleretic action of cholecystokinin and cholecystokinin octapeptide in dogs.

Mongrel dogs were prepared by cholecystectomy, ligation of the lesser pancreatic duct, and insertion of gastric and duodenal cannulas. The common bile duct was cannulated through the duodenal fistula for bile collection while the enterohepatic circulation of bile salts was maintained by intravenous infusion of sodium taurocholate. Cholecystokinin (CCK) and cholecystokinin octapeptide (CCK-OP) caused increased bile flow and had no influence on the biliary clearance of erythritol. The results indicate that the predominant mechanism of CCK and CCK-OP choleresis is due to ductular stimulation.

Animals↗
PubMed1978

Species specificity of cholecystokinin in gut and brain of several mammalian species.

Immunoreactive intact cholecystokinin and its COOH-terminal octapeptide are found in brain as well as in extracts of gut of the monkey, dog, and pig, by using an antiserum with equivalent sensitivities for detecting the octapeptide in free form or incorporated in the intact molecule. The failure to detect intact cholecystokinin in extracts from monkey or dog by using an antiserum developed by immunization with porcine cholecystokinin is presumed to be due to marked species differences in the NH2-terminal portion of the molecule. Tryptic digestion converted the intact cholecystokinin from all species to a peptide resembling the COOH-terminal octapeptide. The amount of cholecystokinin in the brain is comparable to that found in the gastrointestinal tract, the traditional site for this peptide.

Animals↗
PubMed1978

Localization of cholecystokinin-like immunoreactivity in isolated nerve terminals.

Subcellular fractionation of the rat cerebral cortex demonstrated the presence of immunoreactive cholecystokinin in the pellet identified by electron microscopy as containing a high proportion of synaptic vesicles. The recovery in this pellet of 40% of the total immunoreactivity in the initial cortical extract is quite comparable to the recovery of other peptides such as vasoactive intestinal polypeptide and somatostatin, which are also located in synaptosomes and for which roles as neuroregulators or transmitters have been suggested. The evidence of concentration of cholecystokinin-like peptides in the synaptosomal pellet is consistent with our earlier demonstration by immunohistochemical techniques of cholecystokinin's presence in rabbit cerebral cortical neurons. These observations and the evidence for diminished concentration of cholecystokinin-like peptides in the brains of hyperphagic mice are consistent with cholecystolinin's suggested role as a neuroregulator for appetite.

Animals↗
PubMed1978

Effect of chronic pentagastrin, cholecystokinin, and secretin on pancreas of rats.

Pentagastrin (1.5 mg/kg), 20% pure natural cholecystokinin (CCK, 37.5 Ivy dog U/kg) or secretin (25 microgram/kg) was given in a depot carrier subcutaneously to rats 3 times daily for 15 days. The dose of CCK and secretin was submaximal for pancreatic secretion, whereas the dose of pentagastrin was supramaximal for gastric acid secretion. The pancreatic wet weight increased by 12% (P less than 0.01) in the rats treated with pentagastrin, 57% (P less than 0.001) in those treated with CCK, and 9% (P less than 0.01) in those treated with secretin. In CCK-treated rats, the maximal protein and bicarbonate outputs in response to cholecystokinin increased proportionately to the increase in pancreatic weight, but maximal bicarbonate and protein outputs in response to secretin were unaltered. The secretin-treated rats showed a lowered basal secretion of bicarbonate and a lowered sensitivity to secretin stimulation, but the maximal bicarbonate and protein outputs to secretin and CCK were unchanged. Treatment with pentagastrin produced no significant changes in pancreatic responses to secretin or CCK. We conclude that 1) the increase in pancreatic weight produced by repeated injections of cholecystokinin was accompanied by proportional increase in functional capacity as reflected by the increased maximal bicarbonate and protein outputs in response to cholecystokinin, and 2) repeated administration of secretin decreased the sensitivity of the pancreas to secretin without altering maximal bicarbonate response.

Animals↗
PubMed1979

Age-dependent inhibition of suckling by cholecystokinin.

The effects of exogenous cholecystokinin (10--40 U/kg body wt) on neonatal rat suckling were studied in 5-, 10-, 15-, and 20-day-old rats that were equipped with tongue cannulas. Milk (0.1 ml over 10 s) was delivered through the tongue cannula once every minute, providing a rat was still suckling. Cholecystokinin, a well-established inhibitor of adult rat feeding, did not reduce milk intake volume of 5- and 10-day-old rats. It did, however, depress milk intake of 15- and especially of 20-day-old rats. Despite its effect on milk intake, cholecystokinin never lengthened the latency to attach to the nipple and, paradoxically, reduced it on certain occasions. The implications of these findings for the events controlling various aspects of suckling behavior throughout the course of the nursing-suckling period in rats and for the mechanism of action of cholecystokinin are discussed.

Aging↗
PubMed1977

Effects of parenteral secretin--cholecystokinin and of duodenal acid perfusion on gastric secretion in duodenal ulcer patients.

The effect of parenteral secretin-cholecystokinin and duodenal acid perfusion on broth-stimulated gastric acid secretion was studied in 11 duodenal ulcer patients. Statistically significant inhibition occurred in both experimental conditions. The effect of secretin-cholecystokinin was more marked than the effect of duodenal acid perfusion. A poorly responsive subgroup of patients appeared to be responsible for the diminished inhibitory effect of duodenal acid perfusion. In this poorly responsive group there was a diminished duodenal volume response as well as diminished duodenal acid clearing. We conclude that there may exist a diminished release of gastrointestinal hormones such as secretin and cholecystokinin in certain duodenal ulcer patients.

Adult↗
PubMed1977

Cholecystokinin cholecystography in the diagnosis of chronic acalculous cholecystitis and biliary dyskinesia. A cirtical appraisal.

Now that the active fragment of the cholecystokinin molecule has been made available for use in clinical pracitce, reports on the value of cholecystokinin cholecystography must be re-evaluated to determine if the procedure is worthwhile in patients with persistent symptoms and a normal conventional oral cholecystogram. Such an analysis discloses that there is no uniform agreement on what consitutes an abnormal examination and raises serious questions concerning the scientific validity of much of the data. It is apparent that there is no immutable evidence to date to indicate that cholecystokinin cholecystography is an accurate technique to determine which patients in this category will benefit from cholecystectomy.

Adolescent↗
PubMed1977

Cholecystokinin and its COOH-terminal octapeptide in the pig brain.

Two components--one resembling intact cholecystokinin in size and charge and immunologic specificity, and the other resembling the COOH-terminal octapeptide of cholecystokinin--have been found in extracts of the pig cerebral cortex. The relative concentrations of the two peptides in the extracts were dependent on the extractant, boiling 0.1 M HCl being more effective than boiling water for the extraction of intact cholecystokinin but less effective for the extraction of the octapeptide. The physiologic role of these peptides in the brain has yet to be elucidated.

Animals↗
PubMed1978

Characterization of a nontrypsin cholecystokinin converting enzyme in mammalian brain.

An enzyme has been partially purified from canine and porcine cerebral cortical extracts that differs from trypsin in that it manifests some degree of hormone specificity since it converts porcine cholecystokinin to smaller immunoreactive forms, i.e., the COOH-terminal dodecapeptide and octapeptide fragments, but fails to convert big gastrin (34 amino acids) to heptadecapeptide gastrin. This enzyme is distinguishable from trypsin not only in substrate specificity, but also in several physiochemical properties. It is not inhibited in the presence of concentrations of lima bean trypsin inhibitor sufficient to inhibit 1 mg of trypsin per ml of incubation mixture. It is inactivated when incubated with substrate at 45 degrees C for 1 hr, whereas trypsin remains fully active when incubated under the same conditions at 55 degrees C. The enzyme elutes in the void volume on Sephadex G-50 and G-75 gel filtration. On sucrose gradient centrifugation, the proteolytic activity associated with trypsin is recovered above albumin but that of the solubilized brain enzyme is recovered below gamma globulin. The enzyme is not detectable in splenic extracts, which do contain nonspecific proteases capable of completely degrading cholecystokinin. Further investigation is required to determine whether the enzyme in the gut that converts cholecystokinin to the bioactive and immunoactive COOH-terminal fragments resembles or is different from the brain converting enzyme.

Animals↗
PubMed1978

Cholecystokinin inhibits tail pinch-induced eating in rats.

Peripheral administration of the COOH-terminal octapeptide of cholecystokinin in doses from 1 to 100 micrograms per kilogram of body weight (0.25 to 25.0 micrograms per rat) significantly antagonized tail pinch-induced eating in rats, an animal model for stress-induced human hyperphagia. Centrally administered cholecystokinin was effective only in high doses (3 micrograms into the cerebral ventricle). The finding that the minimal effective dose of cholecystokinin in suppressing stress-induced appetitive behavior is smaller after peripheral than central administration suggests that the peptide is acting on peripheral, as opposed to central nervous system, substrates.

Animals↗
PubMed1978

Cholecystokinin inhibits gastric emptying by acting on both proximal stomach and pylorus.

Cholecystokinin is a potent inhibitor of gastric emptying. It is known to both relax the proximal stomach and contract the pyloric sphincter, and either one or both of these actions could mediate inhibition of gastric emptying. We investigated the relative importance of these two actions by studying the effectiveness of the C-terminal octapeptide of cholecystokinin (OP-CCK) to inhibit the emptying of a liquid meal (300 ml saline) before and after operations that either remove or destroy the pyloric mechanism (antrectomy and pyloroplasty), or lead to loss of accommodation of the proximal stomach (vagotomy), and after both vagotomy and antrectomy, and vagotomy and pyloroplasty. The results show that OP-CCK causes dose-related inhibition of gastric emptying in the intact dog. After either pyloroplasty or antrectomy the effectiveness of low but not of high doses of OP-CCK is lost. After vagotomy, OP-CCK at any dose was ineffective. The findings suggest that cholecystokinin inhibits gastric emptying by acting both on the pylorus and on the proximal stomach.

Animals↗
PubMed1979

Gallbladder emptying in response to cholecystokinin. A cholescintigraphic study.

The threshold and dynamics of gallbladder emptying in human subjects in response to cholecystokinin (Pancreozymin, Boots Co. Ltd) were defined by radionuclide imaging with a gamma camera. The radiopharmaceutical employed, 99mTc-HIDA, was taken up rapidly by the liver and efficiently excreted into the biliary system so that gallbladder filling was easily distinguishable from negligible background activity. Counts were recorded continuously on magnetic tape during i.v. infusion of sequentially increasing doses of cholecystokinin: Each dose level was maintained for 15 min. At later playback, the area of interest was adjusted to include only the gallbladder and to exclude radioactivity present in the gut during gallbladder emptying. In 19 normal subjects (10 male and 9 female), a threshold dose of cholecystokin was identified for gallbladder contraction: 0.010 Crick-Harper-Raper units/kg-min in 16 subjects, and 0.020 Crick-Harper-Raper units/kg-min in the remaining 3. The rate of emptying appeared smooth and linear at each dose level: Doubling the dose of cholecystokinin in every case significantly increased the emptying rate. There appeared to be no effect of increasing age on emptying more rapidly than females, but the difference was not significant. This cholescintigraphic technique would appear to offer a simple, accurate, yet noninvasive method for continuously monitoring the events during gallbladder contraction in humans.

Adult↗
PubMed1978

Motility and hemodynamics of the canine gastrointestinal tract. Stimulation by pentagastrin, cholecystokinin and vasopressin.

Effects of pentagastrin (1-4096 ng/kg), cholecystokinin (1-4096 mU/kg, CCK) and vasopressin (.032-128 mU/kg) on gastrointestinal motility and blood flow, were determined by simultaneous measurement of blood flow (electromagnetic flow probes) to and motor activity (strain gages) of corpus, antrum, duodenum, jejunum, and colon of anesthetized dogs. Antral contractile amplitude was increased by pentagastrin at relatively low doses. Pentagastrin also increased corpus blood flow, corpus tone and antral blood flow. Gastric contractile frequency was least sensitive to pentagastrin. Corpus blood flow was decreased and small intestinal blood flow was increased by cholecystokinin at relatively low doses. CCK also increased small intestinal contractile amplitude and, at higher doses, antral contractile amplitude, and duodenal tone. Time-effect relation and sensitivity were different for the hemodynamic and motor responses to pentagastrin and to cholecystokinin. This shows the lack of correlation between vasoactive and motor-stimulating properties of these drugs. However, strong drug-induced contractions were shown to impede antral blood flow (pentagastrin and CCK) by about 35% and duodenal and jejunal blood flow (CCK) by resp. 70 and 60%. Vasopressin reduced blood flow to stomach and intestines by 50-80%, without affecting gastrointestinal motility.

Animals↗
PubMed1979

Localization and molecular heterogeneity of cholecystokinin in the central and peripheral nervous system.

Immunocytochemistry and radioimmunochemistry demonstrate the occurrence of the gastrointestinal hormone cholecystokinin (CCK) in both the central and peripheral nervous system of the guinea pig. CCK nerves are particularly numerous in the neocortex, the hippocampus, the amygdaloid nuclei, the hypothalamus, the spinal cord and in the colon. The nerves contain 5 molecular components of CCK, with gel chromatographical elution constants (Kav) of 0.05, 0.50, 0.90, 1.10 and 1.30, respectively. The four latter correspond to triacontatriapeptide CCK and its COOH-terminal dodeca-, octa- and tetrapeptide portions, respectively. Cholecystokinins are hence widely distributed in the nervous system and occur in the substantial quantities (greater than or equal to 0.2 nmol CCK-8-equiv./g) in several distinct regions.

Animals↗
PubMed1979

Cholecystokinin, amphetamine and diazepam and feeding in lean and obese Zucker rats.

The hyperphagia characteristic of some types of obesity may result from a deficiency in one or more components of the systems controlling satiety which in rats may include the gastrointestinal hormone cholecystokinin (CCK). Obesity may also influence responsivity to often used central nervous system (CNS)-acting drugs and combination of drugs. In these experiments it was shown that: (1) Zucker fatty rats were less sensitive than lean to intraperitoneal injections of 20 U/kg CCK after a 6-hr fast and when reduced were less sensitive than lean and less sensitive than when obese to injections of 5 U/kg CCK; (2) Although fatties were equally sensitive as leans to injections of 0.5 and 1.0 mg/kg d-amphetamine sulfate, when reduced, they were less sensitive; (3) Injections of 1.25 and 2.5 mg/kg diazepam produced smaller increases in food intake after a 6-hr fast in fatty and reduced fatty than lean rats; (4) Combination of diazepam with cholecystokinin in both fatty and lean rats produced feeding similar to that following injection of carrier; and (5) A similar additive effect was obtained in both fatty and lean rats when diazepam was combined with amphetamine; however, the fatty appeared to be more sensitive to the amphetamine than the diazepam effect. Thus the Zucker fatty rat appears to be less sensitive to these chemicals which affect food intake, which supports the contention that their CNS is generally less responsive.

Animals↗