Dysfunction of the gastrointestinal tract. Vasoactive intestinal peptide in peristalsis and sphincter function.
Explore the source record for details and available documents.
Anal Canal↗
SEARCH · PubMed Health
Results for “Vasoactive Intestinal Peptide”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Locomotor activity causes a rapid up-regulation of vasoactive intestinal peptide in the rat hippocampus.
Vasoactive intestinal peptide (VIP) expression is restricted to interneurons in the hippocampus of normal adult rats. However, 3-6 hours after a 60-minute walk in an activity wheel, VIP was transiently expressed in most pyramidal and granular neurons of the hippocampus. Locomotion was also associated with a dramatic increase in VIP immunoreactivity in the motor cortex, primarily in bipolar cells. Reverse transcriptase-polymerase chain reaction analysis indicated that VIP mRNA increases transiently by more than twofold, before the increases in peptide immunoreactivity in both the hippocampus and motor cortex. By comparison, another marker of inhibitory interneurons, glutamate decarboxylase, did not change its expression pattern after locomotion. The calcium binding protein, calbindin-D28K, normally expressed in interneurons, was now found also in glial cells of the hippocampus and motor cortex. Another marker of enhanced electrical activity, the immediate early gene, c-Fos, was expressed in pyramidal and granular neurons at 3 hours but not at 6 hours after locomotion. These results suggest that mapping of peptide expression in the brain of a docile, inactive rat may not reflect the real distribution and functions of a peptide in an active animal.
Animals↗
Calcitonin gene-related peptide II, substance P and vasoactive intestinal peptide in plasma and synovial fluid from patients with inflammatory joint disease.
Immunoreactive plasma and synovial fluid concentrations of calcitonin gene-related peptide II (CGRP II), substance P and vasoactive intestinal peptide (VIP) were measured in patients with osteoarthritis, gout and rheumatoid arthritis. Significantly higher levels of CGRP II and substance P-like immunoreactivity levels in synovial fluid were found in gout as well as CGRP II, substance P and VIP-like immunoreactivities in rheumatoid arthritis when compared to those in osteoarthritis. Plasma CGRP II, substance P and VIP-like immunoreactivity levels showed no significant differences among patients in the three different groups of arthritis. Our results suggest that these neuropeptides released from peripheral nerve endings into the synovial cavity probably play a pathogenic role in human joint inflammation.
Adult↗
Signaling mechanisms of vasoactive intestinal peptide in inflammatory conditions.
The vasoactive intestinal peptide (VIP) is a neuropeptide belonging to the secretin/glucagon family of peptides, which exerts a wide spectrum of immunological functions controlling the homeostasis of immune system through different receptors expressed in various immunocompetent cells. In the last decade, VIP has emerged as a potent anti-inflammatory factor, which exerts its function by regulating the production of both anti- and pro-inflammatory mediators. In this sense, VIP has been proposed as a promising candidate, alternative to other existing treatments, for treating acute and chronic inflammatory and autoimmune diseases, such as septic shock, rheumatoid arthritis, multiple sclerosis and Crohn's disease. The present work reviews the involvement of the specific receptors and or different transduction pathways and transcription factors in the anti-inflammatory action of VIP, and their implication on its therapeutic effect on inflammatory/autoimmune disorders.
Animals↗
Stimulation of sodium and water secretion without inhibition of glucose absorption in the rat jejunum by vasoactive intestinal peptide (VIP).
1. Infusion of vasoactive intestinal peptide (VIP) into the arterial blood supply of the small intestine in anesthetized rats did not alter either the perfusion pressure in the superior mesenteric artery or the active absorption of glucose from the jejunum, but did produce a large net secretion of Na+ and water into the lumen of the jejunum. 2. The results are compared to the effects of prostaglandin E1 which stimulates Na+ and water secretion and inhibits glucose active absorption in the rat jejunum.
Animals↗
Exposure to either gamma or a mixed neutron/gamma field irradiation modifies vasoactive intestinal peptide receptor characteristics in membranes isolated from pig jejunum.
The effect of acute whole body exposure to ionizing radiation was investigated on intestinal vasoactive intestinal peptide (VIP) receptors and adenylate cyclase activity in membranes isolated from pig jejunum. Pigs under light anaesthesia were exposed to a single dose (6 Gy) of gamma (gamma) or to mixed neutron/gamma field (ratio 1:1; neutron/gamma) irradiation. Seven days after irradiation, plasma-membranes were prepared from post mortem jejunal mucosal scrapings. Marker enzyme activities (sucrase, leucine aminopeptidase (LAP), Na,K-ATPase) were measured in each preparation. The characteristics (KD, Bmax) of VIP receptors were determined using 125I-labelled VIP. In addition VIP-sensitive adenylate cyclase activity was measured. Results showed that enzyme activities were reduced following both gamma (sucrase 67%; LAP 53%; Na/K-ATPase 29%; N = 7) and neutron/gamma (sucrase 53%; LAP 59%; Na/K-ATPase 68%; N = 5) compared with control values (N = 5). VIP receptor affinity was decreased following either type of irradiation (gamma or neutron/gamma P < 0.01) and receptor numbers increased. Both VIP- and forskolin-stimulated adenylate cyclase activities were reduced but the sensitivity of the enzyme remained the same for VIP (EC50 values (nmol dm-3)-control-1.27 +/- 0.35; gamma-2.18 +/- 0.41; neutron/gamma-1.91 +/- 0.28). In conclusion, exposure to either gamma or neutron/gamma irradiation attenuates intestinal enzyme activities and VIP receptor affinity but increases VIP receptor numbers.
Adenylyl Cyclases↗
High conservation of upstream regulatory sequences on the human and mouse vasoactive intestinal peptide (VIP) genes.
The neuropeptide vasoactive intestinal peptide (VIP) gene is subject to complex transcriptional regulation resulting in expression of the encoded peptides in distinct subpopulations of neurons in most structures of the nervous system, and tissue-specific changes in expression in response to a variety of hormone and environmental factors. This diverse regulation allows the encoded peptides to carry out putative neurotransmitter, neuromodulator, trophic, neuroendocrine, and immune functions. Despite the potential significance of the processes governing its expression, only the human gene has been studied in any depth, and only a single regulatory element has been identified, a cAMP-responsive sequence less than 100 bp upstream from the transcriptional start site. Because tissue-specific patterns of VIP expression are remarkably well conserved between rodents and humans, we isolated the mouse VIP gene and compared 5' flanking sequences with that of the human gene to identify homologous regions which might be involved in regulation common to both species. Of significant interest is a 210 bp region located more than 1.1 kb upstream from the transcription start site that is 91% conserved between the two species. Of additional interest is a 34 bp perfect dCA.dTG repeat present only on the mouse gene which may be capable of forming Z-DNA.
Animals↗
Pulmonary vascular effects of vasoactive intestinal peptide in conscious newborn lambs.
Vasoactive intestinal peptide (VIP) may be a neurotransmitter in a peptidergic nervous system and is found in nerves in pulmonary blood vessels. Information regarding its pulmonary vascular effects is limited. We therefore studied VIP's effect on pulmonary vascular tone in the immature lung. Normoxic and hypoxic unsedated newborn lambs with chronically implanted flow probes around the right and left pulmonary arteries were used. VIP was injected into one pulmonary artery only, and direct effects of this peptide on the pulmonary vessels were determined by comparing the flow changes in the injected vs. the uninjected lung. VIP was a powerful pulmonary vasodilator with a threshold of 0.3 microgram/kg. It also was a systemic vasodilator (after 1 microgram/kg, aortic pressure fell 27% and cardiac output increased 29%, both P less than 0.01), with a threshold of 0.1 microgram/kg. Pretreatment with propranolol (1 mg/kg iv) did not abolish pulmonary or systemic vasodilation after VIP. On the other hand, pretreatment with indomethacin (3 mg/kg per day for 3 days) abolished VIP-induced pulmonary vasodilation but probably did not affect systemic vasodilation. We conclude that VIP is a powerful pulmonary vasodilator in the newborn lamb and that this dilation can be blocked by the cyclooxygenase inhibitor indomethacin. VIP is also a powerful systemic vasodilator in the newborn lamb but this effect is not blocked by either propranolol or indomethacin.
Animals↗
Stimulation of retinal adenylate cyclase by vasoactive intestinal peptide (VIP).
The effects of vasoactive intestinal peptide (VIP), secretin and glucagon on retinal adenylate cyclase were studied in rabbit, rat and calf retinas. The results demonstrate the presence of a highly active VIP sensitive adenylate cyclase in mammalian retina. The effects are not enhanced by the guanine nucleotide analog 5'-guanylylimidodiphosphate (Gpp(NH)p). Glucagon and secretin also caused significant increases in retinal adenylate cyclase activity although, in general, the magnitude of these effects was less than that of VIP.
Adenylyl Cyclases↗
Behavioral actions of vasoactive intestinal peptide (VIP).
The effect of vasoactive intestinal peptide (VIP) was studied on fear-motivated behaviours, exploration of a novel environment and on novelty and ACTH-induced grooming. VIP was administered via a plastic cannula into the lateral ventricle. Retention of a step-through passive avoidance task was inhibited by 10 and 30 ng VIP injected 1 hour before the retention test. Extinction of pole-jumping active avoidance behaviour was facilitated by 10 and 100 ng VIP. Mild effects were observed in an open field test on exploration and grooming activity. In conclusion, VIP produces inhibitory effects on fear-motivated behaviours.
Adrenocorticotropic Hormone↗
Vasoactive intestinal peptide in human nasal mucosa.
Vasoactive intestinal peptide (VIP), which is present with acetylcholine in parasympathetic nerve fibers, may have important regulatory functions in mucous membranes. The potential roles for VIP in human nasal mucosa were studied using an integrated approach. The VIP content of human nasal mucosa was determined to be 2.84 +/- 0.47 pmol/g wet weight (n = 8) by RIA. VIP-immunoreactive nerve fibers were found to be most concentrated in submucosal glands adjacent to serous and mucous cells. 125I-VIP binding sites were located on submucosal glands, epithelial cells, and arterioles. In short-term explant culture, VIP stimulated lactoferrin release from serous cells but did not stimulate [3H]glucosamine-labeled respiratory glycoconjugate secretion. Methacholine was more potent than VIP, and methacholine stimulated both lactoferrin and respiratory glycoconjugate release. The addition of VIP plus methacholine to explants resulted in additive increases in lactoferrin release. Based upon the autoradiographic distribution of 125I-VIP binding sites and the effects on explants, VIP derived from parasympathetic nerve fibers may function in the regulation of serous cell secretion in human nasal mucosa. VIP may also participate in the regulation of vasomotor tone.
Cells, Cultured↗
Vasoactive intestinal peptide in cerebrospinal fluid.
Immunoreactive vasoactive intestinal peptide (VIP) was measured in lumbar and ventricular cerebrospinal fluid (CSF) from patients with various neurological disorders and in 2 hour aliquots of cisternal fluid removed continuously from rhesus monkeys. Although most of the VIP in concentrated pools of human ventricular fluid and of monkey cisternal fluid co-eluted with synthetic porcine VIP28 on a column of Sephadex G-25 superfine, there was evidence that smaller immunoreactive fragments were also present. A circadian pattern of CSF VIP concentration was observed in 2 of the 3 monkeys studied, with highest levels occurring at night and lowest during the day. Ventricular fluid VIP levels were highest in hydrocephalic children and lowest in patients with multiple sclerosis or epilepsy, while VIP was not detectable in ventricular fluid from patients in coma following a severe head injury. There were no significant differences in VIP concentrations in CSF from patients with dystonia. Parkinson's disease, or Alzheimer's disease, suggesting that VIP containing neurons are not affected in these disorders. Lumbar fluid VIP levels were low in patients undergoing aneurysm surgery. Since VIP is a potent vasodilator, these findings may have important implications in relation to the development of vasospasm following subarachnoid hemorrhage.
Chromatography, Gel↗
Relaxation of muscle strips from the reticular groove and reticulo-omasal orifice by vasoactive intestinal peptide (VIP).
The effect of Vasoactive Intestinal Peptide (VIP) on muscle strips from the reticular groove, the reticulo-omasal orifice (ROO) and the omasal canal was studied. VIP caused a concentration-dependent (10(-8)-5 x 10(-7) mol/l) reduction of the acetylcholine-induced (55 x 10(-6) mol/l) contraction of the reticular groove muscle preparations from calves and adult cattle. VIP was more effective in the muscle strips from calves than in those from adult cattle. Moreover, the circular muscle strips from the reticular groove were more sensitive to VIP than the longitudinal muscle strips. VIP also induced a concentration-related (10(-8)-5 x 10(-7) mol/l) relaxation of muscle strips from the calf ROO. Furthermore, both circular and longitudinal muscle strips from the omasal canal of the calf were relaxed by VIP (10(-7)-5 x 10(-7) mol/l). The relaxing effect of VIP on the circular muscle strips from the reticular groove of the calf was not significantly affected during incubation with 5 x 10(-6) mol/l tetrodotoxin. The relaxing effect of VIP therefore seems to be mediated by VIP receptors of smooth muscle cells. These properties of VIP in conjunction with its presence in nerve fibres located in the wall of the reticular groove and ROO are consistent with a role of VIP as inhibitory transmitter in this region of the bovine stomach.
Animals↗
Requirement of oestrogens for the sensitivity of prolactin cells to vasoactive intestinal peptide in rats and man.
Vasoactive intestinal peptide (VIP) is a prolactin-releasing hormone which is involved in the multifactorial modulation of prolactin secretion in mammals. Intravenous injection of VIP (1 microgram/kg) to fertile women increased plasma prolactin levels and heart rate and reduced diastolic pressure. The same treatment to menopausal women caused similar cardiovascular effects but did not modify plasma prolactin levels. In contrast, TRH (200 micrograms, i.v.) induced a significant increase in plasma prolactin levels in both fertile and menopausal women. The relevance of oestrogens in affecting VIP-stimulated prolactin secretion was evaluated in vitro by measuring prolactin release from pituitary cells of control and ovariectomized rats. The sensitivity of rat mammotrophs to VIP, but not to TRH, was completely suppressed 3 or 4 weeks after ovariectomy. Furthermore, implantation of rats with a silastic capsule containing oestradiol-17 beta during ovariectomy, preserved the cell responsiveness to VIP. The prolactin-releasing property of VIP was also restored when pituitary cells from ovariectomized rats were cultured for 3 days in the presence of 10 nmol oestradiol-17 beta/l before being used for prolactin release experiments. The present study shows that the ability of prolactin-secreting cells to respond to the stimulatory action of VIP requires high levels of circulating oestrogens, both in man and rats.
Adult↗
NFAT interactions with the vasoactive intestinal peptide cytokine response element.
The vasoactive intestinal peptide cytokine response element (VIP CyRE) is responsible for mediating the transcriptional induction of the VIP gene to the neuropoietic cytokines leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF). In investigating the sequence and function of the CyRE, we found a region of DNA with homology to the distal NFAT site in the IL-2 promoter. In this paper we characterize this sequence and show that the VIP NFAT site recognizes T cell NFAT with similar affinity to the previously characterized IL-2 NFAT site. However, despite its location in the middle of the CyRE, we find no CNTF/LIF induced binding to it. Instead we show that in NBFL neuroblastoma cells, the calcium ionophore A23187 induces a protein to bind to the VIP NFAT site. This A23187-mediated induction of nuclear protein binding to an NFAT oligonucleotide is dependent on extracellular calcium but not dependent on de novo protein synthesis. Thus, this protein has the characteristics of an NFAT-like protein and is recognized by an NFAT3-specific antiserum suggesting that it is indeed an NFAT protein. The location of the NFAT site in the VIP CyRE suggests that this may be one mechanism through which different signaling pathways engage in cross talk to alter VIP gene transcription.
Animals↗
Effects of lesions of the suprachiasmatic and paraventricular nuclei on the inhibition of pulsatile luteinizing hormone release by exogenous vasoactive intestinal peptide in the ovariectomized rat.
Vasoactive intestinal peptide (VIP) inhibits pulsatile luteinizing hormone (LH) secretion in the ovariectomized rat. Hypothalamic nuclei known to contain VIPergic neurons were destroyed electrolytically to determine whether either an increased response or a loss of response to exogenous VIP would result. Bilateral electrolytic lesions were made of either the suprachiasmatic (SCN) or paraventricular (PVN) nuclei in separate experiments; all animals received an intracerebroventricular cannula at the same time. Sham-lesioned animals were used as a control. One week later, a catheter was placed in the jugular vein of each rat and, after a recovery period of at least 2 h, blood samples were taken every 5 min for 3 h. After a control period of 1.5 h, either VIP or saline was infused into the third ventricle for an additional 1.5 h. Two doses of VIP were used: 3.5 nmol/h, previously shown to be inhibitory, and 0.4 nmol/h, which is ineffective in ovariectomized rats. LH was measured in the plasma by radioimmunoassay. The high dose of VIP lowered mean LH levels and pulse frequency but had no effect on pulse amplitude in both sham-lesioned and SCN-lesioned rats. The low dose of VIP did not affect pulsatile LH patterns in sham-lesioned rats, but did lower mean LH and pulse frequency in SCN-lesioned rats, indicating a denervation hypersensitivity subsequent to SCN lesions. Destruction of the PVN abolished the inhibitory effect of the high dose of VIP on pulsatile LH release. The low dose of VIP was ineffective in both PVN- and sham-lesioned animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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↗
Somatostatin does not block the effect of vasoactive intestinal peptide on bile secretion in man.
The effects of intravenously administered somatostatin and vasoactive intestinal peptide (VIP) on bile secretion were studied in 10 patients with complete biliary fistulas. The two peptides were administered both separately and simultaneously. During the infusion of vasoactive intestinal peptide, bile secretion increased by 85%, whereas during somatostatin infusion it decreased by 40%. When the peptides were administered together, the VIP-induced choleretic effect was not reduced by somatostatin. Vasoactive intestinal peptide infusion increased bicarbonate concentration and output, whereas somatostatin had the opposite effect. The output of chloride also increased following vasoactive intestinal peptide infusion but decreased following somatostatin infusion. The concentration of chloride was unaffected by somatostatin whereas it was decreased by vasoactive intestinal peptide. The output of bile acids was unaffected by vasoactive intestinal peptide and decreased by somatostatin infusion, whereas total lipid concentration increased during somatostatin infusion and decreased when vasoactive intestinal peptide was added. It is concluded that, in man, somatostatin acts on the bile acid-dependent canalicular bile secretion and also, to some extent, on the ductular secretion, whereas vasoactive intestinal peptide acts strictly at the ductular level. The effects of the two peptides on bile secretion are independent of each other.
Adult↗