Proceedings: Localization of gastric inhibitory peptide, vasoactive intestinal peptide and motilin.
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Interaction of vasoactive intestinal peptide with isolated intestinal epithelial cells from rat. 2. Characterization and structural requirements of the stimulatory effect of vasoactive intestinal peptide on production of adenosine 3':5'-monophosphate.
Porcine vasoactive intestinal peptide stimulated adenosine 3':5'-monophosphate (cyclic AMP) production in rat intestinal epithelial cells. The stimulation was dependent on time and temperature and was potentiated by the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. Under optimal conditions (at 15 degrees C, with 0.2 mM 3-isobutyl-1-methylaxanthine, at a cell concentration up to 18 microgram DNA/ml), the cyclic AMP production produced by vasoactive intestinal peptide was constant for 10 min and stopped after 15 min incubation, at either low (1 nM) or high (30 nM) concentration of the peptide. This plateau effect was demonstrated not to be due to an inactivation of vasoactive intestinal peptide in the medium nor to an alteration of receptors for the peptide. Cyclic AMP production was sensitive to a concentration as low as 0.1 nM vasoactive intestinal peptide. Maximal stimulation of cyclic AMP levels by vasoactive intestinal peptide was observed with 30 nM vasoactive intestinal peptide and represented an 11-fold increased above basal. The dorse-response curve was monophasic with a Km of 2.3 x 10(-9) M. No cooperative effects were detected by Hill analysis. The positive non-linear relationship observed between stimulation of cyclic AMP production and occupancy of binding site was not time-dependent as indicated by experiments performed after 15, 45 and 120 min incubation. Maximal and half-maximal responses were obtained at about 70% and 7% occupation of binding sites, respectively. Chicken vasoactive intestinal peptide and porcine secretin were agonists of porcine vasoactive intestinal peptide with a 6-times and a 120-times lower potency, respectively. Among secretin analogs that were found to have low affinity for vasoactive intestinal peptide binding sites, [4-alanine, 5-valine]secretin, that resembles vasoactive intestinal peptide at the first seven amino acids at the N-terminal end, was a partial agonist of vasoactive peptide at the first seven amino acids at the N-terminal end, was a partial agonist of vasoactive intestinal peptide and others failed to stimulate cyclic AMP production. Glucagon (10microM), gastric inhibitory peptide (0.1 microM), substance, P, neurotensin, octapeptide of cholecystokinin, bovine pancreatic polypeptide, human gastrin I with leucine at residue 15, Leu-enkephalinand somatostatin (1 microM) did not alter cyclicAMP levels. Non-peptide mediators such as dopamine, serotonin, acetylcholine and histamine, tested at 10 microM, were also ineffective. Prostaglandins E2, E1 and isoproterenol, tested at 10 microM, induced an increase of cyclic AMP levels above basal but were 9.5, 13.7 and 17.5 times less efficient than vasoactive intestinal peptide, respectively. Thus vasoactive intestinal peptide is a unique stimulus of cyclic AMP production in rat intestinal epithelial cells.
1-Methyl-3-isobutylxanthine↗
Stimulation of insulin and glucagon secretion by vasoactive intestinal peptide.
In vivo, vasoactive intestinal peptide (VIP) produces simultaneous increases in blood glucose and insulin levels. In order to determine whether VIP, like its homologues, also stimulates insulin secretion directly, studies were made in controlled glucose media employing the vascularly perfused cat pancreas. VIP stimulated insulin secretion significantly in the presence of constant physiological concentrations of glucose. The highest insulin response to VIP (100.3+/-8.1 muU/min) approached the highest insulin response to glucose (119.9 +/- 12.0 muU/min). In the absence of glucose, the insulin response to VIP was insignificant. Unexpectedly, VIP was found to be a more effective stimulant of glucagon than of insulin secretion. The highest glucagon response to VIP (327+/-51% of control levels) was attained in the presence of physiological concentrations of glucose and equalled the glucagon response obtained upon withdrawal of glucose from the perfusate. The glucagon response to VIP was blocked by increasing the glucose in the perfusate. These studies indicate the VIP present in pancreatic islets might play a role in the local control of pancreatic endocrine function.
Animals↗
[Intestinal vasoactive peptide receptors in enterocytes : specific binding and stimulation of cyclic AMP].
Receptors for the vasoactive intestinal peptide (VIP) were characterized on enterocytes isolated from Rat small intestine. Native VIP inhibited competitively the binding of 125I-VIP to enterocytes and strongly stimulated cyclic AMP production; both these effects were observed for concentrations of VIP as low as 0.5-1.0 ng/ml (0.15-0.30 nM) which are compatible with the VIP concentration in the gut.
Animals↗
Interaction of porcine vasoactive intestinal peptide with dispersed pancreatic acinar cells from the guinea pig. Structural requirements for effects of vasoactive intestinal peptide and secretin on cellular adenosine 3':5'-monophosphate.
Secretin and vasoactive intestinal peptide (VIP), but not glucagon, stimulate accumulation of cyclic AMP in dispersed guinea pig pancreatic acinar cells. Secretin stimulated cellular accumulation of cyclic AMP by interacting with a single class of high affinity receptors. On the other hand, the dose-response curve for VIP-stimulated cellular cyclic AMP was biphasic and reflected interaction of this peptide with two classes of receptors. Results obtained with synthetic fragments of VIP and secretin indicate that the receptor having a high affinity for VIP has a low affinity for secretin, interacts with, but does not distinguish among, secretin, secretin 5-27 and [6-tyrosine] secretin or among secretin 14-27, VIP 14-28, VIP 15-28, and increases cellular cyclic AMP when occupied by VIP, but not when occupied by secretin, [6-tyrosine] secretin, or secretin 1-14. The receptor having a low affinity for VIP has a high affinity for secretin, interacts with and distinguishes among secretin, secretin 5-27, and [6-tyrosine] secretin, interacts with secretin 14-27 but not with VIP 14-28 or VIP 15-28, and increases cellular cyclic AMP when occupied by VIP, secretin, [6-tyrosine] secretin, or secretin 1-14.
Animals↗
Hepatic and pulmonary clearance of exogenous vasoactive intestinal peptide in the rat.
1125-labeled vasoactive intestinal peptide (VIP) has been injected into the portal and systemic circulations of rats in an attempt to identify the distribution and fate of the circulating peptide. When VIP I125 was introduced into the portal circulation radioactivity was concentrated in the liver (415.5% +/- 57.2 at 10 min--counts per minute (cpm) per gram of tissue as percentage cpm per milliliter of plasma). Radioactivity in kidney and lung was 346.6% +/- 37.4 and 136.4% +/- 11.4, respectively. In contrast, if the liver was bypassed by performing a portacaval shunt or by injecting into the inferior vena cava, radioactivity was maximal in the lung (2,454.3% +/- 302.3 10 min after IVC injection) with activity in the liver of only 89.3% +/- 10.6. Analysis of the pattern of radioactivity in plasma and tissue extracts by gel filtration chromatography showed the presence of a number of fragments of smaller molecular weight than VIP with a progressive diminution of the amount of VIP-like radioactivity. Both liver and lung have the capacity to concentrate VIP from the circulation. Vasoactive intestinal peptide released into the portal circulation is probably taken up initially by the liver, and this may prevent subsequent uptake by pulmonary tissue. There is some evidence to suggest that the liver and the lung may handle VIP in different ways. If this is so, the enhanced pulmonary extraction of VIP when the liver is bypassed may have some significance for the cardiovascular complications of fulminant liver failure.
Animals↗
Interaction of secretin5-27 and its analogues with hormone receptors on pancreatic acini.
The C-terminal tricosapeptide of secretin (S5-27) and two analogues, one with asparagine replacing aspartic acid in position 15 (15-Asn-S5--27) and one with lysine replacing aspartic acid in position 15 (15-Lys-S5-27) were tested for their abilities to interact with hormone receptors on pancreatic acinar cells. In interacting with the receptors which prefer vasoactive intestinal peptide (vasoactive intestinal peptide-preferring receptors), the apparent affinity of 15-Asn S5-27 was equal to that of 15-Lys-S5-27 and was greater than that of S5-27. In interacting with secretin-preferring receptors, the apparent affinity of 15-Asn-S5--27 was equal to that of S5-27 and was greater than that of 15-Lys-S5-27. In interacting with the secretin-preferring receptors each of the secretin fragments was approximately 2% as effective as secretin in causing an increase in cellular cyclic AMP. None of these fragments was able to cause a detectable increase in cyclic AMP mediated by the vasoactive intestinal peptide-preferring receptors. The dose vs. response curves for the action of secretin and vasoactive intestinal peptide on cellular cyclic AMP and on amylase secretion as well as the pattern of effects of secretin fragments on these actions indicated that the increase in amylase secretion caused by vasoactive intestinal peptide and secretin is mediated exclusively by the vasoactive intestinal peptide-preferring receptors. Furthermore, occupation of approximately 50% of the vasoactive intestinal peptide-preferring receptors is sufficient to cause maximal stimulation of amylase secretion.
Amylases↗
Effects of vasoactive intestinal peptide on glycogenolysis in cultured liver cells.
When isolated rat liver cells were incubated in the presence of vasoactive intestinal peptide at the concentrations ranging from 0.2 microgram to 2 micrograms per ml, glycogenolysis was maximally stimulated within 15 min. However, somatostatin inhibited the liver glycogenolysis. The combined addition to the incubation medium showed that insulin and somatostatin inhibited the stimulated glycogenolysis induced by vasoactive intestinal peptide, while vasoactive intestinal peptide plus secretin showed no additive effect on glycogenolysis, as compared with single the addition of vasoactive intestinal peptide. On the other hand, the additon of glucagon to vasoactive intestinal peptide showed additive effects on glycogenolysis. These results suggest that the receptor site for vasoactive intestinal peptide may be distinguishable from that for glucagon. Extracellular calcium ions were demonstrated to play an important role in the modulation of vasoactive intestinal peptide-induced glycogenolysis. The evidence presented in this paper indicates that glucose metabolism may be partly regulated by the direct action of vasoactive intestinal peptide on hepatocytes, which is referred to as an enterohepatic axis and that the axis is inhibited by insulin and somatostatin.
Animals↗
Hepatic inactivation of vasoactive intestinal peptide in man and dog.
IN AN EFFORT TO DOCUMENT THE ROLE OF THE LIVER IN THE CATABOLISM OF VASOACTIVE INTESTINAL PEPTIDE, SEVERAL DIFFERENT TYPES OF EXPERIMENTS WERE CARRIED OUT, INCLUDING: 1) simultaneous measurement of portal and systemic immunoreactive vasoactive intestinal peptide, both in the basal state and following calcium stimulation; 2) by measuring plasma concentrations of immunoreactive vasoactive intestinal peptide before and after portacaval shunt; 3) by measuring plasma VIP before and after portacaval shunt following calcium, prostigmine and pentagastrin stimulation; 4) by determining plasma VIP levels in patients with liver disease and in hepatic failure, and in patients with variceal hemorrhage before and serially after portal systemic shunt; 5) by measuring CSF vasoactive intestinal peptide in dogs before and after portacaval shunt and when the animals finally succumb to hepatic failure. The results consistently suggest that the shunting of portal blood away from the liver does not result in significant elevation of basal peripheral plasma levels of vasoactive intestinal peptide. Following stimulation however, increased amounts of peripheral plasma VIP are detected, following calcium, pentagastrin and prostigmine release of VIP. Portal vein levels are always significantly higher than peripheral plasma VIP again, confirming a catabolic role for the liver. In patients, elevation of peripheral plasma VIP is seen in hepatic failure, but not after portacaval shunt. Finally, cerebrospinal fluid VIP is elevated in dogs following hepatic failure, confirming the presence of a neural-gut axis and suggesting an influence of hepatic catabolism of VIP not only in the periphery, but also within the central nervous system.
Animals↗
Vasoactive intestinal peptide and its relationship to ganglion cell differentiation in neuroblastic tumors.
Immunohistochemical studies have demonstrated that immunoreactive vasoactive intestinal peptide is present in, and restricted to, the differentiating and mature ganglion cells in a variety of normal and neoplastic neural tissues. In a composite pheochromocytoma-ganglioneuroma (associated with the syndrome of watery diarrhea, hypokalemia, and hypochlorhydria), five ganglioneuroblastomas, five ganglioneuromas (two of which were associated with diarrheal syndromes), an unusual mixed neuroblastoma-ganglioneuroma, and four normal sympathetic ganglia, vasoactive intestinal peptide was present in differentiating and mature ganglion cells. The peptide was also demonstrated in isolated ganglion cells in two pheochromocytomas but was not present in pheochromocytes, Schwann cells, or undifferentiated neuroblastic cells in the neuroblastomas and ganglioneuroblastomas. These studies indicate that the presence and presumably the production of vasoactive intestinal peptide thus reflect a particular line of neuroblastic differentiation and are not merely a reflection of common derivation of these tissues. Our identification of vasoactive intestinal peptide in neurogenic tumors associated with diarrhea supports the contention that the peptide might be an important diarrheogenic factor in these tumors.
Adrenal Gland Neoplasms↗
Possible dual role for vasoactive intestinal peptide as gastrointestinal hormone and neurotransmitter substance.
Vasoactive intestinal peptide (V.I.P.) has been found in high concentrations both in the gastrointestinal tract and, unexpectedly, in the central nervous system. Immunocytochemical studies have demonstrated V.I.P. in nerve-fibers. These findings challenge the concept of V.I.P. as a simple gastrointestinal hormone and suggest a possible neurotransmitter function.
Adrenal Glands↗
Effects of vasoactive intestinal peptide and pancreatic polypeptide on small bowel propulsion in the rat.
Vasoactive intestinal peptide (VIP) and the newly discovered pancreatic polypeptide (PP), both having been proposed as pathogenetic factors in the watery diarrhea syndrome (WDRA), were intravenously infused into rats in order to study the effect on small bowel propulsion. Simultaneously with the infusion of hormone, radioactive test substance was continuously infused into the duodenum of the conscious animal through a permanent catheter. By recording the distribution of radioactivity along the excised gastrointestinal tract, analyses of small bowel propulsion were possible. After infusion of VIP small bowel transit time was significantly prolonged, and the local propagation velocity was retarded both in the proximal and the distal part of the small bowel. PP did not alter small bowel populations. The heavily retarded transport rate after VIP is a propulsive dysfunction and not inconsistent with the clinical sign of diarrhea.
Animals↗
Adrenal tumour secreting vasoactive intestinal peptide and noradrenaline.
A patient with a ganglioneuroblastoma secreting both noradrenaline and vasoactive intestinal peptide is described. Their vasoactive effects are antagonistic and pre-operatively the patient was normotensive. Manipulation of the tumour provoked hypertension and after excision marked hypotension occurred which responded to the administration of metaraminol and blood. This case emphasises the need for thorough investigation of patients with amine or peptide-secreting tumours which have atypical features.
Adrenal Gland Neoplasms↗
Axonal transport of vasoactive intestinal peptide in sciatic nerve.
Dense plexuses of neurones containing immunoreactive vasoactive intestinal peptide (VIP) have been found in discrete areas of the central nervous system and in peripheral organs, including the gastrointestinal tract, pancreas and urogenital system. In many of these locations VIP is concentrated in nerve endings, where it can be released by high K+ concentrations in a Ca2+-dependent manner. VIP release may also be provoked by electrical stimulation of nerves, for example the vagus. VIP thus shows some of the features of neurotransmitter or neuromodulator substances. The presence of immunoreactive VIP in the fine terminal varicosities as well as in the cell bodies of neurones suggests that it might be transported from the perikaryon, where it is presumably formed, to the nerve endings, through the axonal transport system. Such transport would be in keeping with a role for the peptide as a neurohumor or neurohormone. We report here that VIP accumulates in constricted rat sciatic nerves in a manner suggesting fast, anterograde axonal flow.
Animals↗
Potent stimulation of the avian exocrine pancreas by porcine and chicken vasoactive intestinal peptide.
1. The actions of chicken and porcine secretins and vasoactive intestinal peptides (VIPs) were compared on the rate of flow and rate of protein secretion from the exocrine pancreas in urethane anaesthetized turkeys and rats. 2. Chicken VIP was about twice as potent as porcine VIP and 100-150 times as potent as chicken and porcine secretins in stimulating the flow of pancreatic juice in the turkey. 3. Porcine secretin was a strong stimulant of the flow of pancreatic juice in the rat, but chicken secretin and the two VIPs were only active in doses 20-50 times higher than those of porcine secretin. 4. Neither the two VIPs nor the two secretins significantly stimulated the rate of pancreatic protein secretion in the turkey or rat. 5. In the turkey I.V. infusion of graded doses of chicken VIP produced graded increases in the flow of pancreatic juice; in the presence of an infusion of a low dose of CCK8 the flow of juice secreted in response to the highest dose of chicken VIP was significantly lower compared with the infusion of VIP alone, and responses to the other doses of VIP were lower but not significantly so. The infusion of chicken secretin reduced the flow of juice in response to infusions of chicken VIP, but the differences were not significant. There was no significant difference in either the rate of flow, or rate of protein secretion from the turkey pancreas in response to an infusion of chicken secretin and CCK8, compared with CCK8 alone. 6. The results cast doubt on the importance of secretin for regulation of the avian pancreas, and suggest instead that VIP might have a physiological role in regulating the flow of pancreatic juice in birds.
Amino Acid Sequence↗
Effects of vasoactive intestinal peptide on resting and pentagastrin-stimulated lower esophageal sphincter pressure.
Vasoactive intestinal peptide (VIP) administered as an intravenous infusion at different doses (0.8, 1.6, and 3.2 micrograms per kg per hr, respectively) inhibited dose-dependently the response of the lower esophageal sphincter to an intravenous injection of pentagastrin (0.6 microgram per kg) in 4 healthy volunteers. Inhibition ranged from about 20% (not significant) with the low dose to about 55% (P less than 0.05) with the high dose. On the other hand, the VIP doses employed did not substantially decrease basal lower esophageal sphincter pressure. Calculated on the basis of plasma levels of the respective peptides, the inhibitory effect of VIP was about one-third of that of secretin. Even at the smallest dose of VIP, plasma levels of radioimmunoassayable VIP (20 to 100 pmoles per liter) markedly exceeded those encountered normally (1 to 19 pmoles per liter). So, the data presented do not support the suggestion that normally circulating VIP essentially contributes to the physiological regulation of the lower esophageal sphincter pressure; they do not exclude, however, such a role for locally released VIP.
Adult↗
Effects of intravenous vasoactive intestinal peptide (VIP) on gallbladder function in the cat.
The influence of vasoactive intestinal peptide (VIP) on the concentrating mechanism and the motility in the feline gallbladder has been studied in vivo. A perfusion technique made possible a simultaneous study of the motility and of the net transport of water and electrolytes across the gallbladder wall. It was found that an intravenous infusion of VIP relaxes the gallbladder and induces a net fluid secretion into its lumen. The net absorption of chloride ions was markedly reduced, whereas the net transport of sodium, potassium, and bicarbonate was reversed from an absorption into a secretion. Owing to the presence of VIP-containing nerve fibers in the gallbladder wall, a physiological significance for the secretory gallbladder response to VIP is suggested.
Animals↗
Vasoactive intestinal peptide inhibits release of somatostatin from hypothalamus in vitro.
The effect of vasoactive intestinal peptide (VIP) was studied on the release of somatostatin (SRIF) from slices of several regions of the rat brain in vitro. VIP induced a dose-dependent inhibition of SRIF release from mediobasal hypothalamic slices but did not interfere with SRIF release from preoptic area, amygdala or cortex. VIP inhibition had an apparent affinity: Kd = 6.8 +/- 3.9 x 10(-11) M. Secretin had a similar effect but at 600-fold higher concentrations (Kd secretin = 4.2 +/- 0.6 x 10(-8) M). Gucagon was ineffective in concentrations ranging from 10(-10) M to 10(-7) M. The data are consistent with a role of VIP in the hypothalamic control of growth hormone secretion.
Animals↗