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PubMed1993

The SKW 6.4 line of human B lymphocytes specifically binds and responds to vasoactive intestinal peptide.

Vasoactive intestinal peptide (VIP1-28) is a neuromediator recognized by high-affinity receptors on human lymphocytes, which inhibits T-cell proliferation and cytokine secretion, and suppresses immunoglobulin production by mitogen-stimulated mixed mononuclear leucocytes. The direct interactions of VIP1-28 with B cells were studied in the SKW 6.4 line of EBV-transformed human B cells, that express a mean (+/- SD) of 6116 +/- 969 receptors for [125I]VIP1-28 with a mean Kd of 59 nM, that decreases to 12 nM after exposure to phorbol 12-myristate 13-acetate (PMA). The secretion of IgM by SKW 6.4 B cells stimulated optimally with 100 ng/ml of PMA, but not unstimulated secretion of IgM, was suppressed significantly by 10(-12) M to 10(-9) M VIP1-28 and up to a mean maximum (+/- SD) of 40 +/- 2% by 10(-10) M VIP1-28. VIP1-28 elicited concomitant increases in intracellular cyclic AMP up to a mean maximum of 163% at 10(-10) M VIP1-28. The requirement for specific signal transduction by the occupied VIP receptors to inhibit IgM secretion was demonstrated by the lack of effect of VIP4-28 on both cyclic AMP concentration and IgM secretion, despite the equal affinity of binding of VIP4-28 and VIP1-28. The effects of VIP on immunoglobulin secretion by stimulated mixed mononuclear leucocytes thus may be due in part to a direct action on B cells.

B-Lymphocytes↗
PubMed1991

Modulation of neural bronchoconstrictor responses in the guinea pig respiratory tract by vasoactive intestinal peptide.

Vasoactive intestinal peptide (VIP) is localised to cholinergic nerves in airways. We have investigated the effects of VIP on both cholinergic and non-adrenergic, non-cholinergic (NANC) neuronal bronchoconstrictor responses to electrical field stimulation (EFS) in guinea pig airways and on cholinergic neurotransmission following sensory nerve depletion. VIP significantly attenuated the cholinergic bronchoconstrictor responses to EFS in trachea (EC50 values in upper and lower trachea of 3.7 +/- 0.2 x 10(-9) M and 8.6 +/- 0.3 x 10(-9) M, respectively) and bronchi (31.2 +/- 1.6% inhibition in main and 15.1 +/- 3.3% in hilar bronchi at 10(-7) M VIP) and the NANC bronchoconstrictor responses to EFS in bronchi (with maximum inhibitions of 93.1 +/- 1.8% at 3 x 10(-8) M VIP in main and 40.2 +/- 5.3% at 10(-8) M in hilar bronchi). VIP at 10(-7) M, but not at 10(-10) M, significantly attenuated the contractile responses to exogenously applied ACh in trachea (EC50 values of 4.9 +/- 0.2 x 10(-6) M in the absence and 8.4 +/- 0.4 x 10(-5) M in the presence of VIP 10(-7) M VIP) to SP in main bronchi (EC50 values of 5.7 +/- 0.2 x 10(-8) M in the absence vs. 7.3 +/- 0.3 x 10(-7) M in the presence of 10(-7) M VIP). Since the inhibition of these neural responses is greater than the inhibition of the equivalent responses elicited by the exogenous transmitters, this indicates that VIP may modulate release of acetylcholine from cholinergic nerves and of neuropeptides from sensory nerves, in addition to a post-junctional functional antagonist action.

Acetylcholine↗
PubMed1990

Direct coronary vasodilation induced by intracoronary vasoactive intestinal peptide.

Vasoactive intestinal peptide (VIP) is a neurotransmitter that has been identified in epicardial coronary arteries. To evaluate the direct effect of VIP on coronary hemodynamics and blood flow, graded doses of VIP (0.01, 0.03, 0.10, and 0.30 micrograms/min) were infused into the left coronary artery of 7 patients at the time of diagnostic cardiac catheterization for chest pain syndromes. None of the patients had coronary stenoses greater than 50% during subsequent angiography. Coronary sinus VIP concentrations increased during each infusion (22 +/- 28 pg/ml at baseline to 109 +/- 22 pg/ml at 0.30 micrograms/min; p less than 0.05), but arterial VIP was elevated (39 +/- 29 pg/ml) only at the maximal dose of 0.30 micrograms/min. During all dosages of VIP, heart rate, right atrial and left ventricular end-diastolic pressure, and the heart rate x blood pressure product did not change. Moreover, neither mean aortic pressure nor left ventricular peak + dP/dt changed significantly at doses less than 0.30 micrograms/min; at 0.30 micrograms/min, mean aortic pressure decreased (97 +/- 15 to 90 +/- 15 mm Hg; p less than 0.05) and LV peak + dP/dt increased (1,621 +/- 230 to 1,801 +/- 226 mm Hg/s; p less than 0.05). Compared to baseline, the arterial-coronary sinus O2 content difference and myocardial O2 extraction diminished progressively at the 0.03, 0.10, and 0.30 micrograms/min doses of VIP (118 +/- 12 ml O2/L vs. 94 +/- 15, 70 +/- 9, and 61 +/- 26 ml O2/L, respectively, and 0.64 +/- 0.05 vs. 0.53 +/- 0.10, 0.38 +/- 0.06, and 0.34 +/- 0.15, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1976

Choleretic effect of vasoactive intestinal peptide.

Vasoactive intestinal peptide, VIP, was administered intravenously as 10-minute infusions, dosage 0.05 and 0.5 mug/kg/min, to anaesthetized dogs provided with common duct fistulas. When VIP was given to fasting animals, the output of bile, sodium and amylase increased significantly, the bile output by approximately 200% of the control. The biliary concentration of sodium was constant, while that of amylase decreased. When VIP was given to animals, which were fed before the experiment, the bile output was essentially unaffected. The two doses used gave equal peak responses, but the duration of the effect was doubled or trebled following the highest dosage.

Amylases↗
PubMed1995

Quadruple colocalization of calretinin, calcitonin gene-related peptide, vasoactive intestinal peptide, and substance P in fibers within the villi of the rat intestine.

Double-labeling immunofluorescent histochemistry demonstrates that calretinin, a calcium-binding protein, coexists with calcitonin gene-related peptide, vasoactive intestinal peptide, and substance P in the fibers innervating the lamina propria of the rat intestinal villi. An acetylcholinesterase histochemical stain revealed that the majority of calretinin-containing cells in the myenteric ganglia were cholinergic and that about one half of the submucosal calretinin-containing cells colocalized with acetylcholinesterase. In situ hybridization studies confirmed the presence of calretinin mRNA in the dorsal root ganglia, and a ribonuclease protection assay verified the presence of calretinin message in the intestine. The coexistence of calretinin in calcitonin-gene-related-peptide-containing cells that also contained substance P and vasoactive intestinal polypeptide in the dorsal root ganglia suggest that these ganglia are the source of the quadruple colocalization within the sensory fibers of the villi. Although the function of calretinin in these nerves is unknown, it is hypothesized that the coexistence of three potent vasodilatory peptides influences the uptake of metabolized food products within the vasculature of the villi.

Animals↗
PubMed1993

Transmitter role of vasoactive intestinal peptide.

Vasoactive intestinal polypeptide (VIP) is a 28 amino acid with a wide-spread neuronal localization. VIP fulfils many of the classical criteria for neurotransmission. In the cerebral cortex bipolar VIP neurones are involved in the coupling between energy metabolism, blood flow and neuronal activity. Furthermore, VIP in the brain plays a role in circadian rhythms and melatonin and pituitary hormone secretion. In the peripheral nervous system VIP is the transmitter of a number of non-cholinergic, non-adrenergic autonomic events. Thus, the peptide is involved in the control of smooth muscle tone and motility, blood flow and secretion in the digestive tract, respiratory tract and urogenital tract. The effects of VIP are mediated by a specific membrane-bound receptor linked to adenylate cyclase via a stimulatory G-protein. It is likely that impairment of VIP nerves is involved in some autonomic dysfunctions, an example being male impotence which is successfully treated with VIP injections.

Animals↗
PubMed2003

Vasorelaxations induced by calcitonin gene-related peptide, vasoactive intestinal peptide, and acetylcholine in aortic rings of endothelial and inducible nitric oxide synthase-knockout mice.

The objective of this study was to determine if vasorelaxant responses to calcitonin gene-related peptide (CGRP), vasoactive intestinal peptide (VIP), and acetylcholine are altered in aortic rings of mice lacking genetic expression of endothelial nitric oxide synthase (eNOS) or inducible nitric oxide synthase (iNOS) genes (i.e., eNOS- and iNOS-knockout mice) as compared with control (wild-type) mice. Aortic rings from eNOS-knockout (eNOS (-/-)) mice did not relax in response to acetylcholine, thereby confirming previous reports. Aortic rings from iNOS-knockout (iNOS (-/-)) mice relaxed in response to acetylcholine in an endothelium-dependent manner. However, maximum relaxations in endothelium-intact rings were significantly (p < 0.05) larger than in control mice (85.3 +/- 3.1% in iNOS (-/-) mice vs. 67.9 +/- 5.6% in controls). CGRP caused concentration-dependent relaxations in aortas of all three types of mice: control mice, iNOS (-/-) mice, and eNOS (-/-) mice. Vasorelaxant responses to CGRP in control and iNOS (-/-) mice had identical relationships; both were partially dependent on endothelium. In eNOS (-/-) mice, dose-response curves of CGRP in endothelium-intact and endothelium-denuded rings were not significantly different, indicating loss of the partial dependence on endothelium. The vasorelaxant responses to VIP were completely dependent on endothelium in control and iNOS (-/-) mice. Maximum relaxations to VIP in iNOS (-/-) mice (77.4 +/- 2.7%) were significantly greater than in control mice (64.0 +/- 5.5%). Vasorelaxant responses to VIP in eNOS (-/-) aortic rings were also endothelium-dependent, but responses were greatly attenuated compared with wild-type mice. Relaxations induced by VIP (1 x 10 ) in endothelium-intact aortic rings of eNOS (-/-) mice and control mice were 18.3 +/- 5.4% and 64.0 +/- 5.5%, respectively. These findings demonstrated that, in eNOS (-/-) mice, aortic vasorelaxant responses to CGRP were fully present but no longer dependent on the endothelium, and responses to VIP were greatly attenuated compared with control and responses to acetylcholine were abolished. In iNOS (-/-) mice, aortic vasorelaxant responses to VIP and acetylcholine were significantly greater than wild-type control, suggesting that induction of iNOS may have attenuated vascular responses to VIP and acetylcholine in wild-type controls.

Acetylcholine↗
PubMed1998

Interactive mechanisms among pituitary adenylate cyclase-activating peptide, vasoactive intestinal peptide, and parathyroid hormone receptors in guinea pig cecal circular smooth muscle cells.

Vasoactive intestinal peptide (VIP) causes relaxation of smooth muscle cells via both VIP-specific receptor coupled to nitric oxide synthase and VIP-preferring receptor coupled to adenylate cyclase. Because the mechanism of interaction among VIP, pituitary adenylate cyclase-activating peptide (PACAP), and PTH is still unclear, the characteristics of the receptors for PACAP and PTH in circular muscle cells obtained from the guinea pig cecum were investigated. The effects of an inhibitor of cAMP-dependent protein kinase [cyclic adenosine 3',5'-monophosphorothioate (Rp-cAMPS)], guanylate cyclase inhibitors, antagonists of these peptides, and the selective receptor protection on the relaxing effect produced by PACAP, VIP, and PTH were examined. PACAP-induced relaxation was significantly inhibited by a VIP antagonist, a PTH antagonist, Rp-cAMPS, and an inhibitor of particulate guanylate cyclase. VIP-induced relaxation was significantly inhibited by a PACAP antagonist and a PTH antagonist. PTH-induced relaxation was significantly inhibited by a VIP-specific receptor antagonist and Rp-cAMPS, but not by a PACAP antagonist. A PTH antagonist significantly inhibited a VIP-preferring receptor agonist-induced relaxation. The muscle cells in which cholecystokinin octapeptide and PTH receptors were protected completely abolished the inhibitory responses to VIP and PACAP. The muscle cells in which cholecystokinin octapeptide and VIP or PACAP receptors were protected completely abolished the inhibitory response to PTH. This study shows that PACAP induces relaxation of these muscle cells via both VIP-preferring receptor coupled to adenylate cyclase and PACAP-specific receptor, and that PTH induces relaxation of the muscle cells via PTH-specific receptor coupled to adenylate cyclase. In addition, the results of a selective receptor protection show that PTH does not bind to VIP receptors, and that VIP does not bind to PTH receptor. Therefore, this study first demonstrates the presence of one-way inhibitory mechanisms from the PTH-specific receptor to the VIP-preferring receptor, and from the VIP-specific receptor to the PTH-specific receptor in the mechanisms of interaction between VIP and PTH.

Animals↗
PubMed1997

Intraepidermal nerve fiber expression of calcitonin gene-related peptide, vasoactive intestinal peptide and substance P in psoriasis.

In order to evaluate more fully the role of neuropeptides in the pathogenesis of psoriasis, skin biopsies were obtained from 36 patients with psoriasis to identify substance P (SP), vasoactive intestinal peptide (VIP) and calcitonin gene-related peptide (CGRP). Lesional and nonlesional skin was examined from these biopsies and the results compared with those from biopsies taken from patients with a variety of other inflammatory dermatoses, including lichen planus, lichen simplex chronicus, spongiotic dermatitis, and seborrheic dermatitis. Also studied was a series of nine biopsies taken from patients with no known skin disorders. We found an increase in the number of SP-positive nerve fibers within the epidermis in biopsies from lesional skin of psoriasis patients (8.4 nerves per 3-mm biopsy) compared with nonlesional psoriatic skin (2.6 nerves per 3-mm biopsy) and normal skin (2.0 nerves per 3 mm biopsy). Other inflammatory disorders also demonstrated fewer SP-positive nerves than lesional psoriatic skin; lichen planus (0 nerves per 3 mm biopsy) and lichen simplex chronicus (1.3 nerves per 3 mm biopsy). The difference in SP-positive nerve expression between lesional psoriatic skin and the group comprising nonlesional skin, normal skin, lichen planus, and lichen simplex chronicus attained statistical significance (P < 0.013). SP-positive intraepidermal nerve fibers in lesional psoriatic specimens were fewer than in spongiotic dermatitis (17.4 nerves per 3 mm biopsy). There was no significant difference in numbers of VIP- or CGRP-immunopositive intraepidermal nerve fibers between psoriatic skin and the group comprising all other material tested. However, in five patients with psoriasis, there was a marked increase in the expression of intraepidermal CGRP (up to 10.7 nerves per 3-mm biopsy) and VIP (up to 8.3 nerves per 3-mm biopsy) which was not observed in control groups. These findings suggest that neuropeptides SP, CGRP, and VIP play a role in the pathogenesis of psoriasis.

Adult↗
PubMed1989

A peptide histidine isoleucine/peptide histidine methionine-like peptide in the rabbit retina: colocalization with vasoactive intestinal peptide, synaptic relationships and activation of adenylate cyclase activity.

Antisera against peptide histidine isoleucine and peptide histidine methionine were found to label a subpopulation of amacrine and displaced amacrine cells in the rabbit retina with processes ramifying in sublaminas 1, 3 and 5 of the inner plexiform layer. Preadsorption controls demonstrated that this immunoreactivity was specific for a peptide histidine isoleucine- or peptide histidine methionine-like (peptide histidine isoleucine/peptide histidine methionine-like) peptide, and was not caused by cross-reactivity of the peptide histidine isoleucine or peptide histidine methionine antibodies with vasoactive intestinal peptide vasoactive intestinal peptide. In double-label studies, vasoactive intestinal peptide and peptide histidine isoleucine/peptide histidine methionine-like immunoreactivity were colocalized in the same population of retinal neurons. Electron microscopic analysis revealed that the peptide histidine isoleucine/peptide histidine methionine-labelled cells interacted with processes of bipolar cells, amacrine cells and ganglion cells. Peptide histidine methionine and peptide histidine isoleucine were slightly less potent than vasoactive intestinal peptide in stimulating adenylate cyclase activity in the rabbit retina, while the related peptides secretin, glucagon, and the C-terminal vasoactive intestinal peptide fragment, vasoactive intestinal peptide (10-28), showed little or no stimulatory activity. Stimulation of adenylate cyclase by high concentrations of vasoactive intestinal peptide and peptide histidine methionine were non-additive. These results suggest that a peptide histidine isoleucine/peptide histidine methionine-like peptide may function as a neuroactive peptide in the mammalian retina, and that this peptide appears to be cosynthesized and colocalized with vasoactive intestinal peptide and to mimic the activity of vasoactive intestinal peptide through interaction with vasoactive intestinal peptide receptor-adenylate cyclase complexes.

Adenylyl Cyclases↗
PubMed1990

Site specificity of a catalytic vasoactive intestinal peptide antibody. An inhibitory vasoactive intestinal peptide subsequence distant from the scissile peptide bond.

Ten fragments of vasoactive intestinal peptide (VIP) were tested for reactivity with a human catalytic autoantibody that cleaves full-length VIP(1-28) at the Gln16-Met17 peptide bond. A large COOH-terminal subsequence, VIP(15-28), was bound by the autoantibody with high affinity (Ki 1.25 nM), suggesting that it is the antibody binding epitope. VIP(22-28), a short subsequence distant from the scissile bond, inhibited the binding (Ki 242 microM) and hydrolysis (Ki 260 microM) of full-length VIP by the catalytic autoantibody in a competitive fashion. The autoantibody did not show detectable binding of short VIP subsequences that encompass the scissile bond (VIP(15-21), VIP(11-17), and VIP(13-20]. These data show that residues 22-28, located four amino acids distant from the scissile bond, contribute in recognition of VIP by the catalytic autoantibody.

Amino Acid Sequence↗
PubMed1999

Dual actions of S-nitrosylated derivative of vasoactive intestinal peptide as a vasoactive intestinal peptide-like mediator and a nitric oxide carrier.

Vasoactive intestinal peptide (VIP) has been postulated as a non-adrenergic non-cholinergic (NANC) transmitter in the relaxation of vascular and non-vascular systems. In order to synergize the vasoactivities of VIP with nitric oxide (NO), we synthesized a S-nitrosylated derivative of VIP, VIP-Gly-Cys-NO (VIPGC-NO). On aortic rings, VIPGC-NO exhibited a dose-dependent vasorelaxation similar to S-nitrosoglutathione (GSNO), and both induced complete vasorelaxation at 1 microM, whereas, VIP at 1 microM only produced 19% relaxation. The degree of vasorelaxation was proportional to the increases in cyclic GMP with no significant enhancement in cyclic AMP (cAMP) level. On precontracted tracheal rings, VIP, VIPGC-NO, VIPGC and GSNO produced relaxation with EC50 of 74+/-5, 32+/-6, 59+/-9, and 251+/-32 nM, respectively, which was consistent with increases in cyclic GMP (cGMP). A marked increase in cAMP was observed from the tracheal rings pretreated with VIP, VIPGC-NO and its parent VIP-Gly-Cys (VIPGC) as well as isoproterenol. Propranolol only blocked the airway relaxation induced by isoproterenol, but did not antagonize the relaxation induced by VIP, VIPGC and VIPGC-NO. On rabbit sphincter of Oddi, VIP, VIPGC-NO and VIPGC inhibited both basic and acetylcholine-induced contraction frequency and amplitude, whereas, GSNO was less potent than VIP and its derivatives over a range of 2 log units in this respect. On rat gastric fundus, these compounds inhibited contraction amplitude and frequency induced with 5-hydroxytryptamine (5-HT) in the order of inhibitory potency VIP > VIPGC-NO > VIPGC > isoproterenol > GSNO. Our data suggest that: (1) NO is selective in relaxing vascular smooth muscle via the cGMP pathway, whereas VIP is selective in relaxing non-vascular smooth muscles via the activation of both cGMP and cAMP pathways; (2) VIPGC-NO preserves the intrinsic function of VIP but acquires NO-like vasoactivities.

Animals↗
PubMed1990

Peptide histidine valine: its haemodynamic actions and pharmacokinetics in man differ from those of vasoactive intestinal peptide and peptide histidine methionine.

1. The effects of intravenous and intra-arterial infusion of the peptides derived from prepro-vasoactive intestinal peptide, vasoactive intestinal peptide, peptide histidine methionine and peptide histidine valine, were examined in six healthy volunteers. 2. Vasoactive intestinal peptide given intravenously caused a significant increase in heart rate and a decrease in diastolic, but not systolic, blood pressure, whereas peptide histidine valine caused an increase in heart rate alone, despite higher achieved circulating peptide concentrations. Peptide histidine methionine did not affect heart rate or blood pressure. Forearm blood flow was increased by vasoactive intestinal peptide and peptide histidine valine when infused locally intra-arterially, although vasoactive intestinal peptide was more potent than peptide histidine valine. 3. Plasma concentrations of cardiodilatin (the N-terminal peptide derived from pro-atrial natriuretic peptide) were increased by intravenous infusion of vasoactive intestinal peptide, but were unaffected by peptide histidine methionine or peptide histidine valine. Circulating plasma concentrations of adrenaline and noradrenaline did not change during infusion of vasoactive intestinal peptide, peptide histidine methionine or peptide histidine valine. 4. Peptide histidine valine had a long half-life when compared with peptide histidine methionine and vasoactive intestinal peptide. 5. We conclude that peptide histidine valine is active in the human cardiovascular system and has a similar, though less potent, vasodilating action to vasoactive intestinal peptide. The higher circulating levels of peptide histidine valine found in man suggest that it may be important in modulating vascular tone.

Adult↗
PubMed2004

Prevention of experimental autoimmune uveoretinitis by vasoactive intestinal peptide.

BACKGROUND: Vasoactive intestinal peptide (VIP), a neuropeptide that is known to be present in lymphoid tissue microenvironments, shows prominent anti-inflammatory actions. OBJECTIVE: To examine the potential effect of VIP on the development of experimental autoimmune uveoretinitis (EAU). DESIGN: We immunized C57BL/6 mice with human interphotoreceptor retinoid-binding protein peptide 1-20 (h-IRBP peptide). Vasoactive intestinal peptide was administered intraperitoneally on alternate days until day 21 after immunization (entire group). In some cases, VIP was injected at different time points after the induction of immunity with h-IRBP peptide (efferent group). In each experiment, a control group of mice was injected with phosphate-buffered saline instead of VIP. Development of EAU was evaluated by means of histological examination on day 21 after immunization. Furthermore, we determined whether intravenous injection of peritoneal exudate cells cultured with VIP overnight in vitro abrogated EAU. We analyzed delayed hypersensitivity for h-IRBP peptide and the occurrence and severity of EAU using evaluation of histopathological sections for inflammatory ocular disease. RESULTS: Treatment with VIP suppressed the expression of delayed hypersensitivity responses to h-IRBP peptide significantly (positive control vs entire group, P =.02; positive control vs efferent group, P<.001). Mice treated with VIP (n = 10) showed a lower occurrence (40%) and decreased severity of EAU (entire group mean score, 0.3; median score, 0) compared with untreated mice (occurrence, 80%; mean score, 0.85; median score, 0.75), as assessed by histopathological analyses (P =.049). Suppressive effects of VIP on EAU were also observed, even when VIP was administered on days 8 through 20 after immunization (efferent group [n = 9] occurrence, 11%; mean score, 0.1; median score, 0) (P =.003). Moreover, expression of EAU was significantly suppressed when the animals were pretreated with peritoneal exudate cells pulsed with h-IRBP in the presence of VIP (control mean score, 1.2; median score, 1.0; occurrence, 80% [n = 10]) compared with the VIP-treatment group (mean score, 0.3; median score, 0; occurrence, 30% [n = 10]) (P =.004). In addition, VIP-treated peritoneal exudate cells generated regulator T cells in the spleens of recipient mice that were able to interfere with the development of EAU (control group mean score, 0.5; median score, 0.5; occurrence, 63% [n = 8]) compared with the VIP-treatment group (mean score, 0.08; median score, 0; occurrence, 17% [n = 6]) (P =.08). CONCLUSION: Treatment with VIP is a highly effective therapy to suppress EAU. CLINICAL RELEVANCE: As a result of its efficacy in preventing EAU, VIP might be considered as a novel therapeutic modality for human uveitis.

Animals↗
PubMed1993

Lack of effect of three putative vasoactive intestinal peptide receptor antagonists on vasoactive intestinal peptide-induced secretory responses in rat colon.

We have assessed the potential usefulness of three vasoactive intestinal peptide antagonists for investigating whether vasoactive intestinal peptide has a functional role as a secretomotor neurotransmitter at the neuroepithelial junction in rat colonic mucosa. Vasoactive intestinal peptide (VIP) increases short-circuit current in muscle-stripped preparations of rat colon. The response is unaffected by tetrodotoxin and can only be obtained when the peptide is applied to the basolateral side of the membrane. Three putative antagonists were tested for their ability to inhibit short-circuit current responses to vasoactive intestinal peptide. Vasoactive intestinal peptide-(10-28) (1 microM and 3 microM), human growth hormone releasing factor (human GRF) analogue [Ac-Tyr1]human GRF-(1-40)OH (0.1 microM and 1 microM) and [Lys1,Pro2,5,Arg3,4,Tyr6]VIP (0.5 microM) produced concentration-dependent increases in basal short-circuit current but were ineffective as antagonists to vasoactive intestinal peptide.

Animals↗
PubMed1990

Effects of calcitonin gene-related peptide and vasoactive intestinal peptide on nicotine-induced sweating in man.

The effects of two neuropeptides, calcitonin gene-related peptide and vasoactive intestinal peptide on nicotine-induced sweating in human skin were investigated. Intradermal injection of nicotine induced local sweating and each peptide, administered together with nicotine, inhibited these responses in a concentration-dependent manner. The concentration of calcitonin gene-related peptide for threshold and half-maximum inhibition were about 10(-10) M and 10(-8) M, respectively, while those of vasoactive intestinal peptide were approximately 10(-9) M and 10(-7) M, respectively. The results suggest that calcitonin gene-related peptide and vasoactive intestinal peptide have inhibitory effects on the nicotinic action, and release of endogenous calcitonin gene-related peptide and/or vasoactive intestinal peptide may influence sweating in human skin under physiological conditions in vivo.

Adult↗