• Korean Journal of Fisheries and Aquatic Sciences
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• v.38 no.1
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• pp.6-11
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• 2005

Vasopressin (VP)-related peptide was purified from the brain extract of conger eel (Conger myriaster) by reverse-phase, ion-exchange high performance liquid chromatography (HPLC). This peptide with a molecular weight of 1,051.2 Da was determined as $H-Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Arg-Gly-NH_2$, whose Cys residues made an intramolecular disulfide bridge by the automated amino acid sequence analysis, MALDI- TOF mass spectrometry. It's sequence was confirmed by identity of the elution position with the synthetic peptide in HPLC system. As a result of homology investigation, the primary structure of this peptide was the same as that of VP-superfamily member, $[Arg^8]-vasotocin$. The synthetic peptide showed a contractile activity at a minimal effective concentration of $10^{-10}\;M$ on the intestinal smooth muscle of goldfish.

• Journal of Life Science
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• v.29 no.1
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• pp.118-122
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• 2019

Oxytocin (Oxt) and vasopressin (Avp) are mainly synthesized in neuronal cells of the hypothalamus and are released from the posterior pituitary. The structure and sequences of Oxt and Avp genes imply that they are closely related and that they are the result of a duplication event during evolution. A previous study suggested that a small regulatory microRNA (miRNA), miR-24, regulated Oxt after binding. However, it is not clear whether this miRNA can modulate Avp simultaneously. The aim of the present study was to investigate putative targeting miRNAs of Avp, including miR-24. Targeted candidate miRNA oligonucleotides were transfected into COS-7 cells to elucidate the binding activity of miRNAs and Avp using dual-luciferase assays. The luciferase assay showed that only miR-24 displayed elevated binding activity with Avp as compared to a control and other candidate miRNAs. Transfection with seed mutants of Avp and miR-24 inhibitors clearly showed that miR-24 can directly bind to the Avp gene. These results provide new insight into the regulatory mechanism of neurohypophysial hormones by a single miRNA.

• Clinical and Experimental Reproductive Medicine
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• v.48 no.2
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• pp.124-131
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• 2021

Objective: Approximately 30% of preeclamptic pregnancies exhibit abnormal liver function tests. We assessed liver injury-associated enzyme levels and circulating transforming growth factor beta (TGF-β) levels in an arginine vasopressin (AVP)-induced pregnant Sprague-Dawley rat model. Methods: Pregnant and non-pregnant Sprague-Dawley rats (n=24) received AVP (150 ng/hr) subcutaneously via mini-osmotic pumps for 18 days. Blood pressure was measured, urine samples were collected, and all animals were euthanized via isoflurane. Blood was collected to measure circulating levels of TGF-β1-3 isomers and liver injury enzymes in pregnant AVP (PAVP), pregnant saline (PS), non-pregnant AVP (NAVP), and non-pregnant saline (NS) rats. Results: The PAVP group showed significantly higher systolic and diastolic blood pressure than both saline-treated groups. The weight per pup was significantly lower in the AVP-treated group than in the saline group (p<0.05). Circulating TGF-β1-3 isomer levels were significantly higher in the PAVP rats than in the NS rats. However, similar TGF-β1 and TGF-β3 levels were noted in the PS and PAVP rats, while TGF-β2 levels were significantly higher in the PAVP rats. Circulating liver-type arginase-1 and 5'-nucleotidase levels were higher in the PAVP rats than in the saline group. Conclusion: This is the first study to demonstrate higher levels of TGF-β2, arginase, and 5'-nucleotidase activity in PAVP than in PS rats. AVP may cause vasoconstriction and increase peripheral resistance and blood pressure, thereby elevating TGF-β and inducing the preeclampsia-associated inflammatory response. Future studies should explore the mechanisms through which AVP dysregulates liver injury enzymes and TGF-β in pregnant rats.

• The Korean Journal of Pharmacology
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• v.27 no.1
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• pp.21-31
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• 1991

When administered intracerebroventricularly (icv), cholinergic nicotinic agents, nicotine and DMPP, as well as cholinergic muscarinic agents, muscarine and bethanechol, produced pressor responses in urethane-anesthetized vagotomized rabbits. The response patterns to nicotine and to DMPP were similar, while the bethanechol response resembled the muscarine pattern. The pressor response to nicotine and DMPP was markedly inhibited by icv mecamylamine but not by icv pirenzepine, whereas the response to muscarine and bethanechol was inhibited by icv pirenzepine but not by icv mecamylamine, suggesting that both nicotinic and muscarinic receptors in the brain are involved in the action. Intravenous pretreatments of animals with regitine, reserpine, enalapril, saralasin, both regitine and enalapril, both regitine and saralasin, SK&F-100273 did not prevent the pressor response to nicotine and muscarine. Iv pretreatments with both regitine and SK&F-100273 inhibited the nicotine response without affecting the muscarine response, whereas pretreatments with three agents, regitine, enalapril and SK&F-100273, inhibited the muscarine response. The nicotine-induced elevated blood pressure as well as the muscarine-induced were lowered by regitine but not by enalapril or by SK&F-100273. Enalapril was without effect on the nicotine hypertension in rabbits treated with regitine or both regitine and SK&F-100273, whereas SK&F-100273 lowered the nicotine hypertension in regitine-treated animals. Enalapril did not enhance the lowering effect of SK&F-100273 in regitine-treated ones, nor did it cause a fall of the muscarine hypertension induced in regitine-treated rabbits, but it did lower the blood pressure in animals treated with both regitine and SK&F-100273. Likewise, SK&F-100273 did not cause a fall of the muscarine hypertension induced in regitine-treated rabbits, but it did lower the blood pressure in animals treated with both regitine and enalapril. These data suggest that the nicotine-induced hypertensive state is related to at least two systems in the periphery-sympathetic and vasopressin, whereas in the muscarine-induced hypertensive state three systems in the periphery are involved, i.e., the sympathetic, vasopressin and angiotensin system. The hypotensive effect of regitine on basal arterial blood pressure levels of rabbits was not influenced by pretreatment with either of enalapril or SK&F-100273, but significantly potentiated by treating with both enalapril and SK&F-100273, suggesting participation of the sympathetic and the renin-angiotensin system as well as the vasopressin system in maintenance of arterial blood pressure.

• Asian-Australasian Journal of Animal Sciences
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• v.2 no.3
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• pp.273-274
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• 1989

• Proceedings of the Zoological Society Korea Conference
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• 1999.10b
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• pp.255.1-255
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• 1999

No Abstract, See Full Text

• Proceedings of the Zoological Society Korea Conference
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• 1999.10b
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• pp.255.2-255
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• 1999

No Abstract, See Full Text

• The Journal of Pediatrics of Korean Medicine
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• v.29 no.4
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• pp.119-126
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• 2015

Objectives The purpose of this study is to investigate recent clinical studies on effect of acupuncture for Autism Spectrum Disorder in other countries. We have analyzed the studies on effect of acupuncture for Autism Spectrum Disorder within randomized controlled trail (RCT) for 6years (from 2010 to 2015). Methods The search database includes Medline, Embase, Cochrane library and CNKI (China National Knowledge Infrastructure). To narrow the search, the following key search terms were used: 'autism or ASD or Asperger's Syndrome or pervasive developmental disorder, acupuncture'. The search was limited to the publication date from 2010 to 2015. 7 control studies in Medlin, Embase, Cochrane library and 5 control studies in CNKI were selected for analysis. Results and Conclusions 1. The acupuncture and rehabiliation treatment is more effective than only acupuncture treatment. Especially, Retention of needling is helpful. 2. It is necessary to set up standard scale in assessment of ASD patients and serum arginine-vasopressin (AVP) can be substitution. 3. Head acupuncture and tongue acupuncture is effective for ASD.

• The Korean Journal of Physiology
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• v.20 no.2
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• pp.236-248
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• 1986

Alterations of renin-angiotensin system have been suggested as one of the mechanisms increasing arterial blood pressure in experimental and clinical hypertension. But the exact nature of high blood pressure in the early and late phase of renal hypertension is still controversial. To clarify the nature of renin release in both unclipped and clipped kidney of two kidney one clip Goldblatt lypertensive rat, experiments have been done in kidney slices, which were obtained from the rats of 3 and 7 days of operation. Basal rate of renin release was suppressed in unclipped kidney slices compared to clipped kidney Norepinephrine increased renin release from unclipped kidney slices, but not from clipped kidney slices. Suppressions by angiotensin Il and arginine vasopressin of renin release were attenuated in the clipped kidney slices compared to unclipped and sham-operated kidney slices. Increases by verapamil and trifluoperazine of renin release were attenuated in the clipped kidney slices compared to unclipped and sham-operated kidney slices. These results suggest that the negative feedback control mechanism of the renin-angiotensin system by angiotensin Il and arginine vasopressin is attenuated in the clipped kidney of two kidney one clip Goldblatt hypertensive rat, and that one of the altered mechanisms may be caused by certain regulatory changes of intracellular calcium and/or calcium-calmodulin complex in the juxtaglomerular cells.

• The Korean Journal of Physiology
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• v.27 no.1
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• pp.67-77
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• 1993

Acute and chronic effects of ethanol (EOH) administration on the cardiovascular and hormonal responses to repeated hemorrhage were investigated in conscious normotensive Wistar rats and spontaneously hypertensive rats (SHR). The chronic EOH treated group received 5% EOH (vol/vol) ad libitum in the drinking water far the first week,10% for the last 2 weeks, and 20% for the last 5 weeks from the age of 6 weeks. The EOH free group received tap water. Chronic EOH and EOH free groups were randomly subdivided into acute EOH infusion and control groups. Under ether anesthesia, catheters were inserted into the femoral vein and both femoral arteries. After rats regained consciousness and their blood pressure was stabilized, responses to quick hemorrhage (5 ml/kg BW) were tested. In the acute EOH infusion group, hemorrhage was induced 20 min after EOH infusion (1.0 g/kg BW), Baroreceptor reflex sensitivity was assessed by the ratio of changes in hen.1 rate and mean arterial pressure (${\Delta}HR/{\Delta}MAP$) immediately after the hemorrhage. Chronic EOH administration elevated MAP in Wistar rats. During acute EOH infusion, MAP do- creased and HR increased in all groups. In comparison to EOH free control rats, acute or chronic EOH treated rats showed a greater reduction in MAP and a smaller elevation in heart rate in response to a hemorrhage. The degree of MAP reduction was significantly greater in SHR than in Wistar rats. Both the acute and chronic EOH administration attenuated the baroreceptor reflex and retarded MAP recovery, again the trend being much more prominent in SHR. The increase in plasma vasopressin and lenin concentrations after hemorrhage were intensified by the chronic EOH administration. SHR showed a greater vasopressin response but a smaller lenin response than Wistar rats. These results indicate that the EOH treated rats, particularly SHB, are prone to shock by a hemorrhage, which may be partly attributed to an impaired baroreceptor reflex function.