• The Journal of Korean Physical Therapy
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• v.15 no.4
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• pp.442-454
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• 2003

The aim of this study was to demonstrate the effects of silver spike point (SSP) low frequency electrical stimulation on plasma vasoactive intestinal polypeptide (VIP) activities measured by radioimmunoassay from volunteer and the effects of VIP on pain substance-induced contraction investigated by isometric tension methode in animal. The current of 3 Hz continue type, but not 100 Hz continue type, of SSP low frequency electrical stimulation significantly increased in plasma VIP from normal volunteer. The pain substance, such as norepinephrine, serotonin, and prostaglandin $F2{\alpha}$, increased vascular smooth muscle contraction, respectively. These responses were inhibited by VIP applied cumulatively (1 nM - $1\;{\mu}M$), but not serotonin-induced contraction. In addition, serotonin, and prostaglandin $F2{\alpha}$ induced uterine smooth muscle contraction from rat. However, these responses were inhibited by VIP ($1\;{\mu}M$), only serotonin-induced contraction. These results suggest that the VIP regulates pain substance in part and that the SSP low frequency electrical stimulation, specifically current of 3 Hz continue type, significantly increases plasma VIP from volunteer.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.4
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• pp.443-454
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• 1998

The present study was attempted to investigate the effect of vasoactive intestinal polypeptide (VIP) on secretion of catecholamines (CA) and to establish whether there is the existence of a noncholinergic mechanism in adrenomedullary CA secretion from the isolated perfused rat adrenal gland. The perfusion into an adrenal vein of VIP $(3{\times}10^{-6}\;M)$ for 5 min or the injection of acetylcholine (ACh, $5.32{\times}10^{-3}\;M$) resulted in great increases in CA secretion. Tachyphylaxis to releasing effect of CA evoked by VIP was not observed by the repeated perfusion. The net increase in adrenal CA secretion evoked by VIP still remained unaffected in the presence of atropine or chlorisondamine. However, the CA release in response to ACh was greatly inhibited by the pretreatment with atropine or chlorisondamine. The releasing effects of CA evoked by either VIP or ACh were depressed by pretreatment with nicardipine, TMB-8, and the perfusion of $Ca^{2+}$-free medium. Moreover, VIP- as well as ACh-evoked CA secretory responses were markedly inhibited under the presence of $(Lys^1,\;Pro^{2.5},\;Arg^{3.4},\;Tyr^6)-VIP$ or naloxone. CA secretory responses induced by ACh and high $K^+\;(5.6{\times}10^{-2}\;M)$ were potentiated by infusion of VIP $(3{\times}10^{-6}M\;for\;5\;min)$. Taken together, these experimental results indicate that VIP causes CA release in a fashion of calcium ion -dependence, suggesting strongly that there exists a noncholinergic mechanism that may be involved in the regulation of adrenomedullary CA secretion through VIP receptors in the rat adrenal gland, and that VIP may be the noncholinergic excitatory secretagogue present in the chromaffin cells.

• Molecules and Cells
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• v.21 no.3
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• pp.337-342
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• 2006

Interstitial cells of Cajal (ICCs) are pacemaker cells that activate the periodic spontaneous depolarization (pacemaker potentials) responsible for the production of slow waves in gastrointestinal smooth muscle. The effects of vasoactive intestinal polypeptide (VIP) on the pacemaker potentials in cultured ICCs from murine small intestine were investigated by whole-cell patch-clamp techniques. Addition of VIP (50 nM-$1{\mu}M$) decreased the amplitude of pacemaker potentials and depolarized resting membrane potentials. To examine the type of receptors involved in ICC, we examined the effects of the $VIP_1$ agonist and found that it had no effect on pacemaker potentials. Pretreatment with $VIP_1$ antagonist ($1{\mu}M$) for 10 min also did not block the VIP (50 nM)-induced effects. On the other hand exposure to 1H-(1,2,4)oxadiazolo(4,3-A)quinoxalin-1-one (ODQ, $100{\mu}M$), an inhibitor of guanylate cyclase, prevented VIP inhibition of pacemaker potentials. Similarly KT-5823 ($1{\mu}M$) or RP-8-CPT-cGMPS ($10{\mu}M$), inhibitors of protein kinase G (PKG) blocked the effect of VIP (50 nM) on pacemaker potentials as did N-nitro-L-arginine (L-NA, $100{\mu}M$), a non-selective nitric oxide synthase (NOS) inhibitor. These results imply that the inhibition of pacemaker activity by VIP depends on the NO-cGMP-PKG pathway.

• Korean Journal of Veterinary Research
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• v.35 no.3
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• pp.447-458
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• 1995

This study was carried out to characterize nonadrenergic, noncholinergic(NANC) relaxation of porcine retractor penis(PRP) muscle induced by electrical field stimulation(EFS) and to investigate the actions of niric oxide(NO) and vasoactive intestinal polypeptide(VIP) as candidates for NANC neurotransmitters. Biphasic relaxations of PRP muscle were induced by EFS to NANC nerve. Rapid-phase relaxation was observed at low frequency(0.5-16Hz) and slow-phase relaxation followed during high frequency(8-60Hz). Both relaxations were frequency-dependent and TTX($1{\times}10^{-6}M$)-sensitive. L-NAME($2{\times}10^{-5}M$) inhibited the rapid-phase relaxation, but not the slow-phase relaxation. The inhibition of the rapid-phase relaxation with L-NAME was reversed by L-arginine ($1{\times}10^{-3}M$) but not by D-arginine($1{\times}10^{-3}M$). Methylene blue($4{\times}10^{-5}M$) reduced the rapid-phase relaxation. Exogenous No(ExoNO, $1{\times}10^{-5}-1{\times}10^{-4}M$) induced dose-dependent relaxations of PRP muscle. Oxyhemoglobin($5{\times}1^{-5}M$) blocked the relaxation induced by ExoNO and inhibited EFS-induced relaxation. Hydroquinone($1{\times}10^{-4}M$) also abolished the relaxation induced by ExoNO, but did not affect EFS-induced relaxation. L-NAME resistant slow-phase relaxation to EFS was inhibited by ${\alpha}$-chymotrypsin(2.5 U/ml). Both methylene blue($4{\times}10^{-5}M$) and Nethylmaleimide($1{\times}10^{-4}M$) reduced the slow-phase relaxation by EFS. [4-Cl-D-$Phe^6$, $Leu^{17}$]-VIP($3{\times}10^{-6}M$) inhibited the slow-phase relaxation by EFS. External applications of VIP ($1{\times}10^{-7}M$) caused relaxations that were simillar to the L-NAME resistant slow-phase relaxations induced by EFS, and relaxant effects of exogenous VIP were blocked by ${\alpha}$-chymotrypsin(2.5 U/ml).

• The Korean Journal of Pharmacology
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• v.31 no.2
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• pp.219-231
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• 1995

Vasoactive intestinal polypeptide(VIP) and ${\beta}-adrenergic$ agonists have immunomodultory effects on the peripheral blood T-lymphocytes of rat through their own receptors. Both of them utilize the same signal transduction pathway. That is, the stimulatory guanine nucleotide binding protein(G protein) mediates the receptor-adenylyl cyclase coupling, producing intracellular increase of cyclic adenosine monophosphate(cAMP). In the previous experiment, propranolol, a ${\beta}-adrenergic$ receptor blocker, inhibited the VIP-induced protein phosphorylation in lymphocytes. However, propranolol could not block the effect induced by forskolin. Therefore, this study was designed to elucidate the mechanism of the inhibitory action of propranolol on the effects of VIP. Using peripheral blood lymphocytes of rats, the effect of propranolol on the receptor binding characteristics of VIP was observed. And the effects of propranolol were compared to the effects of timolol on the cAMP increase induced by isoproterenol, VIP or forskolin. The results obtained are as follows. 1) Receptor binding study showed no significant differences in the affinity or density of VIP receptor between the control and propranolol-pretreated groups. 2) VIP-induced increase of cAMP was inhibited by propranolol, but not by timolol. 3) Both propranolol and timolol suppressed the isoproterenol-induced cAMP increase. 4) Propranolol also inhibited the histamine-induced cAMP increase. 5) Propranolol did not inhibit the increase of cAMP stimulated by forskolin. 6) Lidocaine did not block the VIP-induced cAMP increase. These results show that the inhibitory mechanism of propranolol is not related to ${\beta}-adrenergic$ receptor or its membrane stabilizing effect, and it is suggested that propranolol can block the effects of VIP by inhibiting the intermediate step between the VIP receptor and adenylyl cyclase.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.217-217
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• 1996

The putative role of vasoactive intestinal polypeptide (VIP) as non-adrenergic non-cholinergic (NANC) neurotransmitter has been studied in rabbit corpus cavernosum. In the presence of atropine and guanethidine the short and prolonged electrical field stimulation (EFS, 2～16 ㎐) induced a frequency-dependent relaxation which was abolished by tetrodotoxin (0.3 ${\mu}$M), a nerve conductance blocker. The neurogenic relaxant reponses were not affected in the presence of VIP-inactivating peptidase, ${\alpha}$-chymotrypsin (2 units/$m\ell$), whereas VIP-induced relaxation were completely abolished. Inhibition of nitric oxide synthase by N$\^$G/-nitro-L-arginine (10～100 ${\mu}$M) caused concentration-dependent inhibition to the neurogenic relaxant responses and at 100 ${\mu}$M the relaxations were virtually abolished. In contrast NO (3～30 ${\mu}$M) and VIP (0.001～l ${\mu}$M)-induced relaxation were unaffected. The inhibitory effect of L-NNA was reversed in the presence of L-arginine (5 mM), the precursor of the NO biosynthesis. Hemog1obin (20～60 ${\mu}$M), sequestering NO in the extracellular space, abolished the NO-evoked relaxation and also caused a concentration-dependent inhibition to the neurogenic relaxation. These observation indicate that NANC relaxation induced by prolonged EFS of rabbit corpus cavernosum is also mediated mainly by nitric oxide as same as that of short EFS, and suggest that VIP is not involved in NANC relaxation of rabbit corpus cavernosum and NO would not be produced by VIP in this tissue.

• Restorative Dentistry and Endodontics
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• v.25 no.2
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• pp.225-234
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• 2000

The purpose of this study was to investigate the distribution and fluorescene intensity of vasoactive intestinal polypeptide(VIP) immunoreactive cells in rat trigeminal ganglion after inferior alveolar nerve axotomy. The animals were divided into normal and two experimental groups. The experimental animals were sacrificed at 14th and 28th day after inferior alveolar nerve axotomy. The trigeminal ganglion was removed and immersed in the 4% paraformaldehyde-0.2% picric acid in 0.1M phosphate buffer. Serial frozon sections about $16{\mu}m$ in thickness were cut with a cryostat. The immunofluorescence staining was performed. The rabbit anti-VIP(1 : 8,000) was used as primary antibody and fluorescene isothiocynate(FITC)-conjugated anti-rabbit IgG(1 : 80) as secondary antibody. The slides were observed under confocal laser scanning microscope. Three-dimensional images were constructed from 9 serial images(each $1{\mu}m$ in thickness) made by automatic optical sectioning. Unprocessed optical sections were obtained and stored on a optical disk. Color picture were printed by a video copy processor. The results were as follows; 1. The appearance of VIP immunoreactive cells in the mandibular part of trigeminal ganglion was 8.79${\pm}$1.99% in normal group and 39.16${\pm}$5.62% in 14 days, 16.25${\pm}$2.39% in 28 days after inferior alveolar nerve axotomy groups. 2. The relative fluorescence intensity of VIP immunoreactive cell bodies in the mandibular part of trigeminal ganglion was 134.40${\pm}$10.39 in normal group and 192.88${\pm}$14.06 in 14 days, 143.10${\pm}$5.02 in 28 days after nerve axotomy groups. Therefore, the relative fluorescence intensity of 14 days after nerve axotomy group was 43.3% higher than intensity of normal group. 3. In optical single section analysis of VIP immunoreactive cell bodies, white cell bodies(moderate fluorescence intensity) were the most abundant in normal and 28 days after nerve axotomy groups. Whereas, in 14 days after nerve axotomy group, red cell bodies(high fluorescence intensity) were the most abundant. 4. In optical serial section analysis of VIP immunoreactive cell bodies, red cell bodies(high fluorescence intensity) were observed in a part of the 9 sections of normal and 24 days after nerve axotomy groups. Whereas, red cell bodies were observed in all of the 9 sections of 14 days after nerve axotomy group. 5. The results indicates that number and fluorescence intensity of VIP immunoreactive cells were increased in the mandibular part of trigeminal ganglion following inferior alveolar nerve axotomy.

• BMB Reports
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• v.47 no.7
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• pp.369-375
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• 2014

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a pleiotropic bioactive peptide that was first isolated from an ovine hypothalamus in 1989. PACAP belongs to the secretin/glucagon/vasoactive intestinal polypeptide (VIP) superfamily. PACAP is widely distributed in the central and peripheral nervous systems and acts as a neurotransmitter, neuromodulator, and neurotrophic factor via three major receptors (PAC1, VPAC1, and VPAC2). Recent studies have shown a neuroprotective role of PACAP using in vitro and in vivo models. In this review, we briefly summarize the current findings on the neurotrophic and neuroprotective effects of PACAP in different brain injury models, such as cerebral ischemia, Parkinson's disease (PD), and Alzheimer's disease (AD). This review will provide information for the future development of therapeutic strategies in treatment of these neurodegenerative diseases.

• Animal cells and systems
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• v.4 no.1
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• pp.95-100
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• 2000

The regional distribution and relative frequencies of endocrine cells were studied immunogistochemically (PAP methods) in the alimentary tract of the tree frog, Hyla areorea japonica, using specific antisera against serotonin, somatostatin, bovine Sp-1/chromogranin (BCG), cholecystokinin (CCK)-8, vasoactive intestinal polypeptide (VIP), gastrin, bombesin, secretin and pancreatic polypeptide (PP). Six kinds of endocrine cells were identified in this study, These immunoreactive cells were located in the gastric glands of stomach regions and in the basal portion of the epithelium of the intestinal tract or esophagus with variable frequencies. They were spherical or spindle-shaped. Serotonin-immunoreactive cells were observed in the whole alimentary tract including the esophagus. Somatostatin-immunoreactive cells were also detected throughout the alimentary tract except the rectum. CCK-8-immunoreactive cells were observed from the pylorus to ileum. Vip-immunoreactive cells were restricted to the rectum. Bombesin-immunoreactive cells were restricted to the fundic gastric regions and gastrin-immunoreactive cells were restricted to the pylorus. However, no BCG-, secretin and PP-immunoreactive cells were demonstrated in this study. In conclusion, the regional distribution and relative frequency of the endocrine cells in the alimentary tract of the tree frog were similar to other anuran species, but some differences which may be caused by feeding habits and species specification were also observed.

• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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• v.10 no.1
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• pp.37-42
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• 1999

The vocal fold has three major function-phonation, respiration and protection, and is richly innervated. The vocal 1314 its autonomic innervation-adrenergic and cholinergic from superior cervical ganglion and the vagus nerve, respectively. The action of both system account for vasoregulation and glandular activity. In e vocal fold several kin of neuropeptides, including SP, CGRP, VIP, TH, NPY, ENK have been reported at the animal including cat or dog. But information regarding the distribution of autonomic nerve fibers containing neuropeptides in the human vocal fold is lacking. Two neuropeptides are of special interest : 1) vasoactive intestinal polypeptide(VIP)that is known to be contained in the parasympathetic(cholinergic) neuron. 2) tyrosine hydroxylase(TH)is located in the cytoplasm of noradrenergic neuron and is the rate-limiting enzyme in noradrenaline synthesis. To understand specific autonomic function of vocal fold we did immunohistochemical examination of VIP and TH in the human vocal fold.