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PubMed1989

Effects of GTP analogs and dithiothreitol on the binding properties of the vascular vasoactive intestinal peptide receptor.

Previous studies have demonstrated a specific vascular receptor for the neurotransmitter peptide, vasoactive intestinal peptide (VIP), and have suggested that the receptor is positively coupled to vascular adenylate cyclase. The present study addressed the questions whether the vascular VIP receptor is subject to regulation by guanine nucleotides and whether a disulfide reducing agent, dithiothreitol, would perturb the binding function of the vascular VIP receptor. Guanosine triphosphate (GTP) and its non-hydrolyzable analogs, guanylyl imidodiphosphate (Gpp(NH)p) and guanosine-5'-O-(3-thiotriphosphate) (GTP-gamma-S), increased the rate of dissociation of radiolabeled VIP from arterial receptors in a concentration-dependent manner. GTP-gamma-S increased the equilibrium dissociation constant (KD) of the high affinity vascular VIP binding site, a result consistent with decreased high affinity binding of VIP induced by GTP-gamma-S. These results are consistent with a regulatory role for guanine nucleotides in the function of the vascular VIP receptor. The disulfide reducing agent, dithiothreitol, caused a decrease in specific binding of radiolabeled VIP. Upon Scatchard analysis the effect of dithiothreitol was characterized by an increase in the KD and a decrease in the maximum number of binding sites (Bmax) of the high affinity binding site. These results suggest that disulfide bonds are important for ligand binding to vascular VIP receptors. The sulfhydryl alkylating agents, N-ethylmaleimide and iodoacetamide, had minimal effects on radioligand binding.

Animals↗

PubMed2001

Vasoactive intestinal peptide: cardiovascular effects.

Vasoactive intestinal peptide (VIP) is present in the peripheral and the central nervous systems where it functions as a nonadrenergic, noncholinergic neurotransmitter or neuromodulator. Significant concentrations of VIP are present in the gastrointestinal tract, heart, lungs, thyroid, kidney, urinary bladder, genital organs and the brain. On a molar basis, VIP is 50-100 times more potent than acetylcholine as a vasodilator. VIP release in the body is stimulated by high frequency (10-20 Hz) nerve stimulation and by cholinergic agonists, serotonin, dopaminergic agonists, prostaglandins (PGE, PGD), and nerve growth factor. The VIP peptide combines with its receptor and dose-dependently activates adenylyl cyclase. The vasodilatory effect of VIP in different vascular tissues or species also may be due to increases in nitric oxide, cyclic GMP, and other signaling agents. In the heart, VIP immunoreactive nerve fibers are present not only in the epicardial coronary arteries and veins, but also the sinoatrial node, atrium, interatrial septum, atrioventricular node, intracardiac ganglia, and ventricles (right ventricle >> left ventricle). In the coronary arterial walls, VIP may contribute to the regulation of normal coronary vasomotor tone. In research animals and in humans, VIP, administered into the coronary artery or intravenously, increases the epicardial coronary artery cross-sectional area, decreases coronary vascular resistance, and significantly increases coronary artery blood flow. High frequency parasympathetic (vagal) nerve stimulation also releases endogenous VIP in the coronary vessels and heart and significantly increases coronary artery blood flow. In addition, the release of VIP in the heart is increased during coronary artery occlusion and during reperfusion where VIP may promote local blood flow and may have a free-radical scavenging effect. VIP also has a primary positive inotropic effect on cardiac muscle that is enhanced by its ability to facilitate ventricular-vascular coupling by reducing mean arterial pressure by 10-15%. In concentrations of 10(-8)-10(-5) mol, VIP augments developed isometric force and increases atrial and ventricular contractility. The presence of VIP-immunoreactive nerve fibers in and around the sinus and the atrioventricular nodes of mammals strongly suggests that this peptide can affect the heart rate. In this regard, endogenously released or exogenous VIP can significantly increase the heart rate and has a more potent effect on heart rate than does norepinephrine. The presence and significant cardiovascular effects of VIP in the heart suggests that this peptide is important in the regulation of coronary blood flow, cardiac contraction, and heart rate. Current investigations are defining the physiological role of VIP in the regulation of cardiovascular function.

Animals↗

PubMed1989

Characterization of autoantibodies to vasoactive intestinal peptide in asthma.

Vasoactive intestinal peptide (VIP) is a potent relaxant of the airway smooth muscle. In this study, VIP-binding autoantibodies were observed in the plasma of 18% asthma patients and 16% healthy subjects. Immunoprecipitation studies and chromatography on DEAE-cellulose and immobilized protein G indicated that the plasma VIP-binding activity was largely due to IgG antibodies. Saturation analysis of VIP binding by the plasmas suggested the presence of one or two classes of autoantibodies, distinguished by their apparent equilibrium affinity constants (Ka). The autoantibodies from asthma patients exhibited a larger VIP-binding affinity compared to those from healthy subjects (Ka 7.8 x 10(9) M-1 and 0.13 x 10(9) M-1, respectively; P less than 0.005). The antibodies were specific for VIP, judged by their poor reaction with peptides bearing partial sequence homology with VIP (peptide histidine isoleucine, growth hormone releasing factor and secretin). IgG prepared from the plasma of an antibody-positive asthma patient inhibited the saturable binding of 125I-VIP by receptors in guinea pig lung membranes (by 39-59%; P less than 0.001). These observations are consistent with a role for the VIP autoantibodies in the airway hyperresponsiveness of asthma.

Adult↗

PubMed1987

Characterization of vasoactive intestinal peptide receptors by a photoaffinity label. Site-specific modification of vasoactive intestinal peptide by derivatization of the receptor-bound peptide.

The biological effects of vasoactive intestinal peptide (VIP) are mediated by binding to a membrane-bound receptor. Probes designed to trap this receptor by binding to it in a covalent way may suffer from a greatly reduced affinity. We report here, for the VIP receptor, the use of a photoaffinity probe obtained by derivatization of receptor-bound VIP with para-azidophenylglyoxal. This method protected the parts of the molecule essential for receptor binding. The VIP derivative thus obtained became covalently linked when irradiated. In the dark, however, it exhibited normal VIP-like behavior and retained its biological activity. This derivatization method might be generally applicable when hormone analogues have to be prepared without loss of receptor affinity. Receptor characterization studies on liver plasma membranes showed the presence of high- and low-affinity binding sites with KD = 0.1 and 5 nM, respectively. Treatment of membranes with dithiothreitol causes loss of high-affinity binding. The high-affinity site, trapped by the photoaffinity probe, resolved into two molecular mass forms, 50 and 200-250 kDa. Reduction of the receptor-probe complex left the 50-kDa form intact, whereas the amount of the 200-250-kDa form greatly diminished. We demonstrate the importance of the presence of disulfide bonds in one of the molecular forms involved in high-affinity binding.

Affinity Labels↗

PubMed1986

Coexistence of calcitonin gene-related peptide and vasoactive intestinal peptide in cholinergic sympathetic innervation of rat sweat glands.

Immunoreactivity for calcitonin gene-related peptide (CGRP) has been localized with indirect immunofluorescence techniques in the cholinergic sympathetic fibers that innervate eccrine sweat glands in the rat. This innervation also contains vasoactive intestinal peptide-like immunoreactivity (VIP-IR). A small proportion of principal neurons in stellate and lumbar sympathetic ganglia which provide innervation to the sweat glands contain detectable CGRP-immunoreactivity. The CGRP-IR neurons are immunoreactive for VIP; however, many VIP-IR neurons in these ganglia do not contain detectable levels of CGRP-IR.

Animals↗

PubMed1987

Vasoactive intestinal peptide and intraocular pressure: adenylate cyclase activation and binding sites for vasoactive intestinal peptide in membranes of ocular ciliary processes.

Vasoactive intestinal peptide (VIP)-responsive adenylate cyclase and VIP binding sites were investigated in membranes prepared from ciliary processes dissected from albino rabbit eyes. High-affinity binding sites for VIP (Kd, 0.95 nM; 607 fmol/mg of protein), in addition to beta adrenergic sites labeled by dihydroalprenolol (Kd, 0.48 nM; 123 fmol/mg of protein), were present. Activation of adenylate cyclase by VIP had a Ka of 65 nM, and the maximal response was 3.3-fold greater than that for I-isoproterenol (Ka, 102 nM). A peptide fragment of VIP (sequence 10-28) was inactive in all assays and did not inhibit VIP-stimulated adenylate cyclase at 10 microM. Responses to VIP and isoproterenol in combination were additive at lower doses but less than additive at maximal doses. Responses to VIP in combination with a low dose of forskolin (0.1 microM) were potentiated at all dose levels, whether assays were done in presence of MgCl2 or MnCl2. VIP- and forskolin-activated adenylate cyclase was associated with the nonpigmented epithelial cell fraction and not with pigmented epithelial cells separated on Percoll density gradients after dissociation of cells from processes by collagenase digestion. Intravitreous injection of 10 nmol of VIP into the rabbit eye caused a maximal reduction in intraocular pressure at 40 to 50 hr lasting beyond 72 hr. VIP-responsive and beta adrenergic-responsive adenylate cyclase are present on the same cell type (nonpigmented epithelial cells) and appear to share components of the adenylate cyclase system in the same membrane. VIP may participate in the physiologic regulation of aqueous humor secretion at the level of the epithelial cell membrane.

Adenylyl Cyclases↗

PubMed1987

Ontogenic development of vasoactive intestinal peptide receptors in rat intestinal cells and liver.

Changes in the functional and biochemical characteristics of membrane receptors for vasoactive intestinal peptide (VIP) were evaluated in vitro, using epithelial intestinal cells isolated during rat development, from day 17 of gestation to adulthood. These characteristics included cell cAMP generation, adenylate cyclase and cAMP-dependent phosphodiesterase cAMP-PDE activities, [125I]VIP-binding capacity, and the molecular components of [125I]VIP-binding sites. In 19-day-old fetuses, VIP induced a significant and persistent increase in cAMP production, which lasted for 10 min in intestinal cells. This effect, measured at 37 C in the absence of cAMP-PDE inhibitor, only lasted for 3 min in 5-day-old rats and was undetectable in adult intestine. Addition of the cAMP-PDE inhibitor 3-isobutyl-1-methylxanthine with VIP caused, potentiated, and maintained elevated cAMP levels at the three stages considered. Intestinal cells were more sensitive to VIP in 17- and 19-day-old fetuses (ED50 = 5 and 17 X 10(-11) M VIP, respectively, at 15 and 37 C) than in adult rats (EC50 = 2.7 and 1.6 X 10(-9) M VIP). Adenylate cyclase activity rose 4-fold in fetal intestine and had an apparent Ka of 4 X 10(-10) M VIP. These changes in VIP receptor activity were not observed for PGE2 receptors in developing rat intestinal cells or in the VIP-sensitive adenylate cyclase system prepared from liver of fetuses and adults. They might be due to differences between the molecular components of the intestinal VIP receptor, which were identified here as autoradiographic bands of 64,800 daltons in 19-day-old rat fetuses and 74,600 daltons in adults (P less than 0.01). Alternatively, the changes in VIP receptor activity in 5-day-old rats may result from decreases in the number and affinity of the [125I]VIP-binding sites and increases in the velocity of cAMP-PDE activity. The release of VIP from intestinal nerve endings during fetal and postnatal development and the absorption of VIP from milk might, therefore, modulate the intestinal VIP receptor and its effector systems. Because specific VIP receptors were expressed before the morphological and functional differentiation of intestinal and liver cells, we conclude that their activity is an indicator of their development, and suggest that in rats, this neuropeptide may regulate the maturation and functions of intestine and liver during fetal life.

Aging↗

PubMed1993

Vasoactive intestinal peptide release and L-citrulline production from isolated ganglia of the myenteric plexus: evidence for regulation of vasoactive intestinal peptide release by nitric oxide.

Vasoactive intestinal peptide release and L-[3H]citrulline production were examined in ganglia isolated from the myenteric plexus of guinea-pig intestine. The nicotinic agonist, 1,1-dimethyl-4-phenylpiperizinium stimulated vasoactive intestinal peptide release and L-[3H]citrulline production; the latter was considered an index of nitric oxide production. Both vasoactive intestinal peptide release and L-[3H]citrulline production were abolished by tetrodotoxin, hexamethonium, and the nitric oxide synthase inhibitor, NG-nitro-L-arginine. Inhibition of vasoactive intestinal peptide release by NG-nitro-L-arginine was reversed by L-arginine but not by D-arginine. Exogenous nitric oxide stimulated vasoactive intestinal peptide release whereas exogenous vasoactive intestinal peptide had no effect on L-[3H]citrulline production. The pattern of stimulation by nitric oxide and inhibition by NG-nitro-L-arginine implied that vasoactive intestinal peptide release is facilitated by and may be dependent on nitric oxide production. Consistent with this notion, vasoactive intestinal peptide release in response to either 1,1-dimethyl-4-phenylpiperizinium or nitric oxide was abolished by KT 5823, an inhibitor of cyclic GMP-dependent protein kinase activity and by LY83583, an inhibitor of soluble guanylate cyclase activity. The study provides the first direct evidence of nitric oxide production from enteric ganglia.

Alkaloids↗

PubMed1988

A comparison of the differential effects of vasoactive intestinal peptide and peptide histidine isoleucine on the vascular and capsular smooth muscle of the dog spleen.

1. The actions of the two peptides, vasoactive intestinal peptide (VIP) and peptide histidine isoleucine (PHI) have been compared to that of isoprenaline on the smooth muscle systems of the isolated blood-perfused dog spleen. 2. Intra-arterial injections of VIP and PHI caused graded increases in splenic arterial blood flow at constant perfusion pressure indicative of splenic arterial vasodilatation. 3. VIP was significantly more potent than PHI, with their respective molar ED50 values being 9.9 +/- 3.7 and 830 +/- 141 pmol (P less than 0.002). VIP was approximately 10 and 200 times more potent than isoprenaline and PHI respectively. 4. The maximum reduction in splenic arterial vascular resistance was the same (P greater than 0.5) in response to intra-arterial VIP and PHI, although both peptide maxima were significantly less (P less than 0.05, 0.01 respectively) than that obtained with isoprenaline. 5. Small increases in spleen volume accompanied the splenic vasodilator responses to both peptides. They were probably passive in origin, secondary to splenic arterial vasodilatation. 6. The selective beta 2-adrenoceptor antagonist, ICI 118,551, did not antagonize the splenic arterial vasodilator response to VIP or PHI but markedly attenuated the effect of isoprenaline. 7. These observations indicate that VIP and PHI, when either co-released locally or present together in the systemic circulation, may exert a differential action on different components of the circulation.

Adrenergic beta-Antagonists↗

PubMed2001

Expression and fine mapping of murine vasoactive intestinal peptide receptor 1.

Vasoactive intestinal peptide (VIP) plays multiple roles in the nervous, endocrine, and immune systems as a neurotransmitter, a hormone, and a cytokine. VIP is widely distributed in neurons of the central and peripheral nervous systems (CNS/PNS), and recently has been found to be an important neuroprotective agent. VIP actions are mediated through specific G protein-coupled receptors. We have cloned the cDNA of VIP receptor subtype 1 (VIPR1 or VPAC1) and have demonstrated the quantitative expression profile in mice. Fluorometric real-time reverse transcription-polymerase chain reaction (RT-PCR) analysis demonstrated that VPAC1 is expressed in all tissues examined. Expression was highest in the small intestine and colon followed by the liver and brain. The high level of VPAC1 expression in forebrain and cerebellum suggests that VPAC1 may mediate the neuroprotective effect of VIP. We have refined the chromosomal localization of the mouse, rat, and human VPAC1 genes. This fine mapping of the VPAC1 gene extends the respective regions of synteny between the distal region of mouse chromosome 9, rat chromosome 8q32, and human chromosome 3p21.33-p21.31. Thus, VPAC, constitutes a functional-positional candidate for the tumor-suppressor function mapped to human 3p22-p21 where loss-of-heterozygosity is observed in small-cell lung carcinoma (SCLC) cell lines and primary tumors. Availability of the cDNA sequences for mouse VPAC1 will facilitate the generation of VPAC1 null mutant animals. Such studies will ultimately enhance our understanding of the role of VIP in the nervous system.

Amino Acid Sequence↗

PubMed1995

Structure, expression, and chromosomal localization of the type I human vasoactive intestinal peptide receptor gene.

Vasoactive intestinal peptide (VIP) and other members of the pituitary adenylyl cyclase-activating peptide (PACAP) and secretin neuroendocrine peptide family are recognized with specificity by related G protein-coupled receptors. We report here the cloning, characterization, and chromosomal location of the gene encoding the human type I VIP receptor (HVR1), also termed the type II PACAP receptor. The gene spans approximately 22 kb and is composed of 13 exons ranging from 42 to 1400 bp and 12 introns ranging from 0.3 to 6.1 kb. Primer extension analysis with poly(A)+ RNA from human HT29 colonic adenocarcinoma cells indicated that the transcription initiation site is located at position -110 upstream of the first nucleotide (+1) of the translation start codon, and 75 nt downstream of a consensus CCAAT-box motif. The G+C-rich 5' flanking region contains potential binding sites for several nuclear factors, including Sp1, AP2, ATF, interferon regulatory factor 1, NF-IL6, acute-phase response factor, and NF-kappa B. The HVR1 gene is expressed selectively in human tissues with a relative prevalence of lung > prostate > peripheral blood leukocytes, liver, brain, small intestine > colon, heart, spleen > placenta, kidney, thymus, testis. Fluorescence in situ hybridization localized the HVR1 gene to the short arm of human chromosome 3 (3p22), in a region associated with small-cell lung cancer.

Adenocarcinoma↗

PubMed1987

Immunohistochemical detection of ganglia in the rat stomach serosa, containing neurons immunoreactive for gastrin-releasing peptide and vasoactive intestinal peptide.

Ganglia, not previously described, were identified in the rat stomach serosa along the minor curvature. The ganglia consisted of varying number of cell bodies lying in clusters along or within nerve bundles. The ganglia were shown to contain GRP and VIP immunoreactive nerve fibers and cell bodies and also some NPY immunoreactive fibers, whereas they were devoid of somatostatin immunoreactivity. Nerve ligation experiments indicated that the ganglia are intrinsic to the stomach.

Animals↗

PubMed1991

Neonatal androgenization increases vasoactive intestinal peptide levels in rat anterior pituitary: possible involvement of vasoactive intestinal peptide in the neonatal androgenization-induced hyperprolactinemia.

Accumulating evidence suggests that vasoactive intestinal peptide (VIP) may be a physiological PRL-releasing factor. In the present study, we examined a possible involvement of VIP in the neonatal androgenization (NA)-induced hyperprolactinemia. Twenty-four hours after birth, newborn female rats were injected sc with 1,000 micrograms of testosterone (NA) or with oil vehicle only (control). Both groups were sacrificed at 8 weeks of age. Compared to controls, NA rats showed significantly higher plasma PRL levels (7.3 fold), anterior pituitary (AP) PRL content (2.1 fold) and plasma estradiol levels (2.1 fold). AP VIP content was extremely higher (61 fold) in NA rats than in controls. However, NA did not affect VIP content in the suprachiasmatic nucleus, paraventricular nucleus or median eminence. These results suggest that the NA-induced hyperprolactinemia may be mediated, at least in part, by paracrine and/or autocrine effects of the increased AP VIP on PRL secretion. However, since the potentiation by NA of the AP VIP content was extremely marked compared to those of the other parameters, the possibility was also raised that the increased AP VIP may be involved in other endocrine and/or nonendocrine events occurring in the AP.

Androgens↗

PubMed1989

Vasoactive intestinal peptide: behavioral effects in the rat and hamster.

The behavioral effects of intracerebroventricular (ICV) injection of the brain-gut peptide vasoactive intestinal peptide (VIP) were quantified with a behavioral sampling technique in home-caged, nondeprived, male and female albino rats and golden hamsters. ICV VIP sex-dependently decreased observed resting behavior during 1 hr after injections in both rats and hamsters at 0.1-10.0 micrograms. Grooming behavior was increased in hamsters, and rearing and standing behaviors were increased in rats, sex-dependently at VIP doses that decreased resting. Drinking behavior was suppressed in rats by VIP at 10.0 micrograms. Intraperitoneal (IP) VIP (100.0 micrograms/kg) increased 5% ethanol intake and decreased eating behavior in fluid-deprived male rats. The increase in ethanol intake produced by IP VIP was prevented by IP cholecystokinin octapeptide (CCK, 4.0 micrograms/kg). VIP potently controls resting and ingestive behaviors, suggesting a role for this neuropeptide, along with CCK, in the feedback regulation of rodent behavior.

Alcohol Drinking↗

PubMed2005

Vasoactive intestinal peptide in the amygdala inhibits tail flick reflexes in rats.

The present study was conducted to test the capability of a representative type of non-opioid peptides vasoactive intestinal peptide (VIP) in the amygdala to modulate nociception. Bilateral application of VIP into the basolateral region of the amygdala persistently suppressed radiant heat-evoked tail flick reflexes of anesthetized rats. The present result suggests that VIP synapses in the amygdala may play important roles in controlling pain, as with opioid synapses in the amygdala. This result also implies that local VIP in the amygdala is likely to subserve activating the descending antinociceptive systems of the brainstem from the amygdala.

Amygdala↗

PubMed2000

Effect of growth hormone releasing hormone (GHRH) and vasoactive intestinal peptide (VIP) on in vitro bovine oocyte maturation.

The aim of this study was to investigate the effects of growth hormone releasing hormone (GHRH) and the structural-related peptide vasoactive intestinal peptide (VIP) on nuclear maturation, cortical granule distribution and cumulus expansion of bovine oocytes. Bovine cumulus oocyte complexes (COCs) were cultured in M199 without FCS and gonadotropins and in the presence of either 100 ng/mL bovine GHRH or 100 ng/mL porcine VIP. The COCs were incubated at 39 degrees C in a humidified atmosphere with 5% CO2 in air, and the nuclear stage was assessed after 16 or 24 h of incubation using DAPI staining. Cortical granule distribution was assessed after 24 h of incubation using FITC-PNA staining. To assess the effects of GHRH and VIP on cumulus expansion, COCs were incubated for 24 h under the conditions described above. In addition, 0.05 IU/mL recombinant human FSH was added to GHRH and VIP groups. Cultures without GHRH/VIP/FSH or with only FSH served as negative and positive controls, respectively. At 16 h neither GHRH (42.9%) nor VIP (38.5%) influenced the percentage of MII stage oocytes compared with their respective controls (44.2 and 40.8%). At 24 h there also was no difference in the percentage of MII oocytes between GHRH (77.0%), VIP (75.3%) and their respective controls (76.0 and 72%). There was no significant cumulus expansion in the GHRH or VIP group, while FSH induced significant cumulus expansion compared with the control groups, which were not inhibited by GHRH or VIP. Distribution of cortical granules was negatively affected by GHRH and VIP. The percentage of oocytes showing more or less evenly dispersed cortical granules in the cortical cytoplasm aligning the oolemma (Type 3) was lower in the GHRH (2.7%) and VIP (7.8%) groups than in the control group (15.9%). In conclusion, GHRH and VIP have no effect on nuclear maturation or cumulus expansion of bovine COCs but retard cytoplasmic maturation, as reflected by delayed cortical granule migration.

Animals↗

PubMed1999

[Vasoactive intestinal peptide and epidermal growth factor upregulates bcl-2 gene expression in bronchial epithelial cells].

Expression of protooncogenes bcl-2 and c-myc in cultured rabbit bronchial epithelial cell (BEC) was investigated in order to shed some light on genetic mechanisms underlying the protective antioxidant effect of pulmonary regulatory peptides, vasoactive intestinal peptide (VIP) and epidermal growth factor (EGF). Effects of these peptides and heat stress (HS) on expression of these genes were also studied. Total RNA was extracted from BEC. Bcl-2 mRNA and c-myc mRNA were cloned with the method of RT-PCR. GAPDH mRNA was used as internal control. The products of RT-PCR were separated with electrophoresis in 2% agarose gels. A computer image treating system (Stratagene eagleeye II) was used to identify the specific band and evaluate the density. The product bands of target genes bcl-2 were checked with Southern blot and oligoneucleotides probe hybridyzation. The results show: (1) a low level of bcl-2 and c-myc gene transcription occur in BEC at the resting state; (2) both VIP and EGF could promote bcl-2 and c-myc transcription, but no significant change could be found in the HS group; (3) there was a close correlation between bcl-2 and c-myc transcription (r = 0.98. P < 0.01). The above results indicate that VIP and EGF can improve the antioxidant effect of BEC by upregulating bcl-2 gene expression potently modulated by c-myc protein.

Animals↗

PubMed1988

Mechanisms of vasoactive intestinal peptide release in short-term culture of vasoactive intestinal peptide-producing tumor.

Vasoactive intestinal peptide-producing tumor tissue fragments obtained at surgery were maintained in short-term culture. Functional cellular integrity of vasoactive intestinal peptide-producing tumor tissue was reflected by progressive protein synthesis and the ability of tumor tissue to release vasoactive intestinal peptide when stimulated by the intracellular second messengers cyclic adenosine monophosphate and calcium. Studies with verapamil and ethyleneglycol-bis (beta-aminoethylether)-N,N'-tetraacetic acid suggest that cyclic nucleotide- and ionophore A23187-mediated vasoactive intestinal peptide release are dependent, at least in part, upon the availability and transmembrane transport of extracellular calcium.

1-Methyl-3-isobutylxanthine↗