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Peripheral modulation of duodenal and colonic motility and arterial pressure by neuropeptide Y, neuropeptide Y fragment 13-36, peptide YY, and pancreatic polypeptide in rats: cholinergic mechanisms.

The pancreatic polypeptide-fold (PP-fold) peptides neuropeptide Y (NPY), peptide YY (PYY), and pancreatic polypeptide (PP) (500 pmol/kg) increased duodenal and colonic intraluminal pressure of urethane-anesthesized rats following intravenous (i.v.) bolus injections. Increases in mean arterial pressure (MAP) accompanied the excitatory effects of NPY and PYY on gastrointestinal motility in these rats during the same time period. Atropine attenuated PYY's excitatory effect on duodenal pressure of rats. Excitatory effects of NPY, PYY, and PP (i.v.) on rat colon were not mediated via the muscarinic receptors. In the presence of hexamethonium, a nicotinic antagonist, PP (i.v.) increased colonic pressure to a greater extent than when administered alone. This observation suggested that PP had an inhibitory effect on colonic motility, which was not apparent as a result of the larger excitatory component. The nicotinic antagonist did not modulate the effects of peripherally administered NPY or PYY on duodenal or colonic motility in anesthetized rats. The Y2 receptor ligand, NPY (13-36) (i.v.) (500 pmol/kg), increased duodenal and colonic pressure in rats to the same extent as the full NPY molecule. Therefore, the peripheral effect of PYY and NPY on duodenal and colonic motility in rats may be mediated via Y2 receptors. NPY and PYY (i.v.) initially increased MAP, which then return to baseline values. Unlike NPY and PYY (i.v.) which produced short-term hypertensive effects PP (i.v. decreased MAP. Atropine did not attenuate the hypertensive effects of PYY and NPY (i.v.); however, the hypotensive effect of PP (i.v.) was blocked by atropine. The effects of the PP-fold peptides on MAP were not altered in the presence of hexamethonium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1970

Endocrine hormones.

Explore the source record for details and available documents.

Adrenocorticotropic Hormone↗
PubMed1999

The mechanism of histamine secretion from gastric enterochromaffin-like cells.

Enterochromaffin-like (ECL) cells play a pivotal role in the peripheral regulation of gastric acid secretion as they respond to the functionally important gastrointestinal hormones gastrin and somatostatin and neural mediators such as pituitary adenylate cyclase-activating peptide and galanin. Gastrin is the key stimulus of histamine release from ECL cells in vivo and in vitro. Voltage-gated K(+) and Ca(2+) channels have been detected on isolated ECL cells. Exocytosis of histamine following gastrin stimulation and Ca(2+) entry across the plasma membrane is catalyzed by synaptobrevin and synaptosomal-associated protein of 25 kDa, both characterized as a soluble N-ethylmaleimide-sensitive factor attachment protein receptor protein. Histamine release occurs from different cellular pools: preexisting vacuolar histamine immediately released by Ca(2+) entry or newly synthesized histamine following induction of histidine decarboxylase (HDC) by gastrin stimulation. Histamine is synthesized by cytoplasmic HDC and accumulated in secretory vesicles by proton-histamine countertransport via the vesicular monoamine transporter subtype 2 (VMAT-2). The promoter region of HDC contains Ca(2+)-, cAMP-, and protein kinase C-responsive elements. The gene promoter for VMAT-2, however, lacks TATA boxes but contains regulatory elements for the hormones glucagon and somatostatin. Histamine secretion from ECL cells is thereby under a complex regulation of hormonal signals and can be targeted at several steps during the process of exocytosis.

Enterochromaffin Cells↗
PubMed2004

Glucagon-like peptide 1: evolution of an incretin into a treatment for diabetes.

Glucagon-like peptide 1 (GLP-1) is a product of proglucagon that is secreted by specialized intestinal endocrine cells after meals. GLP-1 is insulinotropic and plays a role in the incretin effect, the augmented insulin response observed when glucose is absorbed through the gut. GLP-1 also appears to regulate a number of processes that reduce fluctuations in blood glucose, such as gastric emptying, glucagon secretion, food intake, and possibly glucose production and glucose uptake. These effects, in addition to the stimulation of insulin secretion, suggest a broad role for GLP-1 as a mediator of postprandial glucose homeostasis. Consistent with this role, the most prominent effect of experimental blockade of GLP-1 signaling is an increase in blood glucose. Recent data also suggest that GLP-1 is involved in the regulation of beta-cell mass. Whereas other insulinotropic gastrointestinal hormones are relatively ineffective in stimulating insulin secretion in persons with type 2 diabetes, GLP-1 retains this action and is very effective in lowering blood glucose levels in these patients. There are currently a number of products in development that utilize the GLP-1-signaling system as a mechanism for the treatment of diabetes. These compounds, GLP-1 receptor agonists and agents that retard the metabolism of native GLP-1, have shown promising results in clinical trials. The application of GLP-1 to clinical use fulfills a long-standing interest in adapting endogenous insulinotropic hormones to the treatment of diabetes.

Animals↗
PubMed1977

A comparison of intrinsic nerve supplies of two muscular layers of duodenum.

The duodenums of opossums and cats were cut into strips 2 mm wide and 2-2.5 cm long. Strips cut in the direction of the oral-caudal axis were called longitudinal strips, and those cut at 90 degrees to that axis were called circular strips. Each muscle strip was stimulated with trains of electrical rectangular pulses (10 Hz, 50-70 V, 0.5 ms). In the longitudinal strips, electrical field stimulation caused contraction, and this contraction was abolished by atropine, 10(-7) M. In the circular strips, electrical field stimulation caused relaxation. This relaxation was abolished by tetrodotoxin, 10(-7) M, but it was not affected by antagonists to adrenergic and cholinergic transmission, nor by some gastrointestinal hormones. Reserpinization of the opossums or alteration of the frequencies of electrical field stimulation from 0.1-50 Hz did not affect or alter the relaxation of the circular strips or the contraction of the longitudinal strips. These findings suggest that the longitudinal muscle is dominated by an excitatory cholinergic innervation, and the circular muscle is dominated by a nonadrenergic, noncholinergic inhibitory innervation.

Animals↗
PubMed1996

Pig pancreatic acinar cells possess predominantly the CCK-B receptor subtype.

Studies performed on pig indicated that its pancreas was insensitive to the gastrointestinal hormone cholecystokinin (CCK) and suggested that its secretions were rather under the control of the neurotransmitter acetylcholine. This study was performed to determine reasons for this insensitivity by comparing secretory responses to different secretagogues and establishing the dominant CCK receptor type. Pancreatic acini prepared from weaned piglets were evaluated for their sensitivity to carbamylcholine (Cch), caerulein, JMV-180, and secretin. RNA were extracted for CCK-A and CCK-B receptor expression using specific cRNA probes. Results indicate that pig pancreatic acini are sensitive to Cch and relatively insensitive to caerulein with no response to JMV-180, a CCKA agonist, or secretin; MK-329, a CCK-A receptor antagonist, significantly inhibited caerulein-induced enzyme secretion from 10(-8) M. The pig pancreas expresses few CCK-A mRNA receptors but a majority of CCK-B. These data demonstrate that the pig pancreas expresses a majority of CCK-B receptors. In conclusion, the pig pancreas possesses a large majority of CCK-B receptors responsible for their low sensitivity to CCK.

Amylases↗
PubMed2005

GLP-1 reduces intestinal lymph flow, triglyceride absorption, and apolipoprotein production in rats.

Glucagon-like peptide 1 (GLP-1) is a gastrointestinal hormone secreted in response to meal ingestion by enteroendocrine L cells located predominantly in the lower small intestine and large intestine. GLP-1 inhibits the secretion and motility of the upper gut and has been suggested to play a role in the "ileal brake." In this study, we investigated the effect of recombinant GLP-1-(7-36) amide (rGLP-1) on lipid absorption in the small intestine in intestinal lymph duct-cannulated rats. In addition, the effects of rGLP-1 on intestinal production of apolipoprotein (apo) B and apo A-IV, two apolipoproteins closely related to lipid absorption, were evaluated. rGLP-1 was infused through the jugular vein, and lipids were infused simultaneously through a duodenal cannula. Our results showed that infusion of rGLP-1 at 20 pmol.kg(-1).min(-1) caused a dramatic and prompt decrease in lymph flow from 2.22 +/- 0.15 (SE) ml/h at baseline (n = 6) to 1.24 +/- 0.06 ml/h at 2 h (P < 0.001). In contrast, a significant increase in lymph flow was observed in the saline (control) group: 2.19 +/- 0.20 and 3.48 +/- 0.09 ml/h at baseline and at 6 h of lipid infusion, respectively (P < 0.001). rGLP-1 also inhibited intestinal triolein absorption (P < 0.05) and lymphatic apo B and apo A-IV output (P < 0.05) but did not affect cholesterol absorption. In conclusion, rGLP-1 dramatically decreases intestinal lymph flow and reduces triglyceride absorption and apo B and apo A-IV production. These findings suggest a novel role for GLP-1 in lipid absorption.

Animals↗
PubMed2006

Taste receptors in the gastrointestinal tract. IV. Functional implications of bitter taste receptors in gastrointestinal chemosensing.

Changes in the luminal contents of the gastrointestinal tract modulate gastrointestinal functions, including absorption of nutrients, food intake, and protection against harmful substances. The current notion is that mucosal enteroendocrine cells act as primary chemoreceptors by releasing signaling molecules in response to changes in the luminal environment, which in turn activate nerve terminals. The recent discovery that taste receptors and G protein subunits alpha-gustducin and alpha-transducin, involved in gustatory signal transduction, are expressed in the gastrointestinal mucosa supports the concept of a chemosensory machinery in the gastrointestinal tract. An understanding of luminal sensing processes responsible for the generation of the appropriate functional response to specific nutrients and nonnutrients is of clinical importance since aberrant or unsteady responses to changes in luminal contents might result in disease states ranging from intoxication to feeding disorders and inflammation. The purpose of this theme article is to discuss the functional implications of bitter taste signaling molecules in the gastrointestinal tract deduced by their localization in selected populations of epithelial cells and their relationship with neural pathways responsible for the generation of specific responses to luminal contents.

Animals↗
PubMed1980

Motilin-independent ectopic fronts of the interdigestive myoelectric complex in dogs.

We have studied in four conscious dogs the relationship between circulating concentrations of motilin and the activity front (phase III) of the interdigestive myoelectric complex. During fasting, cyclic peaks of motilin secretion were concomitant in every instance with the initiation of activity fronts that began in the stomach or duodenum. When somatostatin was administered at doses of 5, 2.5, or 0.625 microgram x kg-1 x h-1 for 3 h, motilin concentrations were stabilized at lowered levels and no activity fronts occurred in the duodenum. Somatostatin also inhibited the stimulatory effects of exogenous motilin on the entire small intestine. During somatostatin infusion, however, ectopic fronts began in the jejunum and were propagated to the cecum despite low motilin concentration. After a 100-g meat meal, the cyclic increase of motilin was interrupted and no activity fronts were observed in the duodenum, but ectopic fronts started lower in the small intestine. Our study supports the hypothesis that motilin induces activity fronts in the canine duodenum, but it shows that ectopic fronts are not controlled by motilin.

Action Potentials↗
PubMed1981

Studies on the inhibition of pancreatic secretion by luminal somatostatin.

The effects of somatostatin, instilled into the duodenum or administered intravenously, on pancreatic response to endogenous (meal and duodenal acidification) or exogenous (secretin and caerulein) stimulants were compared in five dogs with gastric and pancreatic fistulas. Somatostatin, whether applied topically to the duodenal mucosa or given intravenously, resulted in qualitatively similar inhibition of pancreatic secretion of water, bicarbonate, and enzyme protein, being about four to eight times less potent after intraduodenal than after intravenous administration. A meal-induced secretion appears to be the most sensitive to the inhibitory action of intraduodenal somatostatin, probably because of the suppression of gastric acid and serum gastrin secretin involved in the postprandial stimulation of the exocrine pancreas. The inhibition of pancreatic secretion by luminal somatostatin was accompanied by a significant increase of plasma levels of the immunoreactive somatostatin, indicating that this peptide can be absorbed intact across the intestinal mucosa. We conclude that somatostatin administered into the gut lumen is absorbed into the circulation and can inhibit pancreatic secretion both by the suppression of the release of gastrointestinal hormones and by direct inhibitory action on the exocrine pancreas.

Animals↗
PubMed1981

Endocrine secretion of alpha-amylase by the pancreas.

The effect of the gastrointestinal hormone, cholecystokinin-pancreozymin (CCK-PZ), on the flux of alpha-amylase across the basolateral surface of the pancreas into interstitial fluid was measured by following its appearance in the medium bathing whole rabbit pancreas in organ culture. CCK-PZ increased the rate of amylase release by about an order of magnitude for the maximum applied dose. The response was only observed at concentrations of CCK-PZ that were supramaximal for ductal enzyme secretion (320 pmol/l to 10 nmol/l). Over this range, amylase secretion into the bath varied widely with dose, whereas that into the duct remained relatively unchanged. These observations, in conjunction with others, suggest that the acinar cell, and not the duct system, is the direct source of this amylase and that there is a natural secretion of digestive enzyme from the acinar cell in the endocrine direction that is augmented by CCK-PZ or a homologous peptide.

Animals↗
PubMed1983

Effect of pancreatic polypeptide on canine migrating motor complex and plasma motilin.

A potential role of pancreatic polypeptide (PP) in the regulation of phase III of the migrating motor complex (MMC) was investigated in conscious dogs before and during bilateral vagal blockade. After a control fasting period, cyclical increments in plasma PP occurred with peak levels of 45 +/- 8 pmol/l coinciding with late phase II MMC motility. By contrast, after food a substantially higher (approximately five times peak fasting concentrations) and more prolonged elevation of PP was observed, in association with a postprandial pattern of activity. To approximate fasting plasma PP concentrations, porcine PP was infused at 100 pmol X kg-1 X h-1, which produced levels of plasma PP of 99 +/- 8 pmol/l. At this dose PP had no effect on phase III activity. However, at a dose of 400 pmol X kg-1 X h-1, which achieved plasma PP concentrations (283 +/- 33 pmol/l) similar to postprandial levels, there was a specific inhibition of phase III in the lower esophageal sphincter, stomach, duodenum, and upper jejunum. The phase III-associated increment of plasma motilin was also inhibited by this dose of PP. These inhibitory effects at the 400 pmol X kg-1 X h-1 dose of PP were also observed after bilateral blockade of the vagus nerves. Our results suggest that PP has no significant role in the modulation of phase III of the fasting MMC nor does it induce a typical feeding motor pattern. The selective inhibition of both phase III and the associated rise in plasma motilin by PP plasma levels similar to postprandial concentrations does, however, point to a possible role for pancreatic polypeptide in the postprandial inhibition of phase III of the MMC.

Animals↗
PubMed1983

Effects of cholecystokinin and secretin on intestinal structure and function.

Cholecystokinin and secretin are believed to be trophic gastrointestinal hormones. Studies were designed to determine whether these hormones exert their effect through stimulation of endogenous secretion. First, four groups of parenterally nourished rats underwent bypass of the proximal two-thirds of the intestine. One group received secretin, another cholecystokinin octapeptide (CCK-OP), another CCK-OP plus secretin, while the fourth group served as control. After 1 wk, animals were killed; pancreas and segments of intestine were removed. First, mucosal weight, protein content, and fatty acid esterification activity were affected only in intestine in continuity with endogenous secretions after hormone administration. Second, the effects of these hormones were tested in chow-fed rats. The hormone-treated group, despite pancreatic hyperplasia, had similar indexes of intestinal mass compared with pair-fed controls. We conclude that CCK-OP and secretin mediate their trophic effects on the small intestine indirectly, probably through stimulation of pancreatic secretion. In addition, the effects of luminal nutrients have complex interactions with these hormones.

Animals↗
PubMed1984

Erythromycin mimics exogenous motilin in gastrointestinal contractile activity in the dog.

The gastrointestinal motor stimulating activity of erythromycin (EM) was studied in conscious dogs. It was found that a 20-min intravenous infusion of EM lactobionate at a dose of 50-100 micrograms (potency) X kg-1 X h-1 induced a group of strong contractions in the stomach and the duodenum, and the contractions migrated along the small intestine to the terminal ileum. The EM-induced contractions were quite similar to the naturally occurring interdigestive migrating contractions (IMC) in the gastrointestinal tract in frequency, contractile force, and duration of the contractions, migrating velocity, and accompanying peaks of plasma motilin concentration. The EM-induced contractions in the stomach were inhibited by feeding and intravenous infusion of pentagastrin (1.5 micrograms X kg-1 X h-1) but were not affected by secretin; these findings are identical to those found with the naturally occurring and motilin-induced contractions. Like motilin, EM stimulated motor activity only during the interdigestive state. We conclude that EM induces IMC associated with the release of endogenous motilin in the dog.

Animals↗
PubMed1991

Regulation of intestinal cholecystokinin and somatostatin mRNA by bombesin in rats.

The neuropeptide bombesin has been shown to stimulate secretion of several gastrointestinal hormones, including cholecystokinin (CCK). We have previously demonstrated that stimulation of CCK release by feeding is associated with an increase in steady-state intestinal CCK mRNA levels. The purpose of the present study was to determine whether bombesin stimulates CCK release in rats and, if so, to determine whether bombesin regulates CCK mRNA levels in a manner similar to that of feeding. To establish a proper dose of bombesin for stimulating CCK release, rats received 1-h intravenous infusions of 0.25, 1, 4, or 16 micrograms.kg-1.h-1 bombesin. Basal plasma CCK levels averaged 1.8 +/- 0.4 pM and increased to peak levels of 2.9 +/- 0.6 pM within 15 min of infusion with 4 micrograms.kg-1.h-1 bombesin (the maximally effective dose). With the use of this dose, rats then received infusions of bombesin or saline lasting up to 24 h. At 1, 2, 4, and 24 h, animals were killed for collection of plasma for CCK measurements and of intestine for measurements of intestinal CCK and somatostatin mRNA levels. Bombesin treatment stimulated an increase in plasma CCK levels at 1 h, but levels declined to basal by 4 h, where they remained at 24 h. Despite increasing plasma CCK levels, bombesin infusion, unlike dietary stimulation, had no effect on duodenal CCK mRNA levels. Finally, to determine whether the decrease in plasma CCK levels after prolonged bombesin treatment was due to tachyphylaxis, rats treated with bombesin for 4 h were also fed soybean trypsin inhibitor (a known stimulus of CCK secretion).(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗
PubMed1992

CCK, bombesin, and carbachol stimulate c-fos, c-jun, and c-myc oncogene expression in rat pancreatic acini.

To identify possible nuclear signals mediating long-term regulation of the pancreas by gastrointestinal hormones, the expression of c-fos, c-jun, and c-myc was investigated in rat pancreatic acini. Stimulation of the acini with cholecystokinin octapeptide (CCK-8, 100 pM), bombesin (10 nM), or carbachol (10 microM), but not gastrin (100 nM), secretin (100 nM), or vasoactive intestinal peptide (10 nM) induced an increase in oncogene mRNA expression. The percent increases of c-fos, c-jun, and c-myc mRNA were 207 +/- 40, 171 +/- 26, and 46 +/- 19 (n = 5) for CCK-8; 223 +/- 71, 159 +/- 31, and 43 +/- 21 (n = 5) for bombesin; and 125 +/- 51, 123 +/- 58, and 67 +/- 19 (n = 5) for carbachol, respectively. CCK-induced increases in oncogene mRNA were rapid and transient. c-fos and c-jun mRNA levels were increased after 30 min stimulation, peaked at 1 h, and returned to basal level in 2 h. Activation of c-myc was more prolonged with levels remaining elevated for at least 3 h. The effects of CCK-8 were concentration dependent. Detectable stimulation was seen at 10 pM; maximal stimulation occurred at 10 nM and was not affected by further increase in the concentration of CCK-8. JMV-180, a high-affinity site CCK receptor agonist and low-affinity site antagonist, alone did not stimulate c-fos mRNA expression but inhibited c-fos mRNA expression induced by CCK-8. These results suggest that the interaction between CCK and the low-affinity state of the CCK receptor is responsible for oncogene activation.

Animals↗
PubMed1995

Gastrin-CCK-B type receptors on human T lymphoblastoid Jurkat cells.

The presence of specific receptors for gastrointestinal hormones on T cells and their involvement in the immune response are still matters of debate. We reported the effects of gastrin-cholecystokinin (CCK)-related peptides on J.RT3-T3.5 Jurkat cells. A single class of high-affinity binding sites (dissociation constant approximately 0.1 nM) for gastrin and CCK-8 was evident on these cells. These peptides dose-dependently induced a transient increase in intracellular Ca2+ concentration ([Ca2+]i), which was independent of extracellular Ca2-. L-365,260 was 150- to 300-fold more potent than L-364,718 to inhibit radiolabeled ligand binding or peptide-stimulated [Ca2+]i increase, confirming the gastrin-CCK-B nature of the receptor. Gastrin caused a rise in inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] level within 5 s of stimulation. Finally, gastrin increased interleukin (IL)-2 secretion in J.RT3-T3.5 cells. We conclude that 1) J.RT3-T3.5 cells possess "gastrin-CCK-B type" receptors coupled to phospholipase C activation, Ins(1,4,5)P3 formation, and Ca2+ release from intracellular Ca2+ pools, and 2) these receptors could be involved in the regulation of IL-2 production.

Calcium↗