• The Korean Journal of Physiology and Pharmacology
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• 제26권4호
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• pp.255-262
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• 2022

Oxytocin is a neuropeptide produced primarily in the hypothalamus and plays an important role in the regulation of mammalian birth and lactation. It has been shown that oxytocin has important cardiovascular protective effects. Here we investigated the effects of oxytocin on vascular reactivity and underlying the mechanisms in human umbilical vein endothelial cells (HUVECs) in vitro and in rat aorta ex vivo. Oxytocin increased phospho-eNOS (Ser 1177) and phospho-Akt (Ser 473) expression in HUVECs in vitro and the aorta of rat ex vivo. Wortmannin, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K), inhibited oxytocin-induced Akt and eNOS phosphorylation. In the rat aortic rings, oxytocin induced a biphasic vascular reactivity: oxytocin at low dose (10^-9-10^-8 M) initiated a vasorelaxation followed by a vasoconstriction at high dose (10^-7 M). L-NAME (a nitric oxide synthase inhibitor), endothelium removal or wortmannin abolished oxytocin-induced vasorelaxation, and slightly enhanced oxytocin-induced vasoconstriction. Atosiban, an oxytocin/vasopressin 1a receptor inhibitor, totally blocked oxytocin-induced relaxation and vasoconstriction. PD98059 (ERK1/2 inhibitor) partially inhibited oxytocin-induced vasoconstriction. Oxytocin also increased aortic phospho-ERK1/2 expression, which was reduced by either atosiban or PD98059, suggesting that oxytocin-induced vasoconstriction was partially mediated by oxytocin/V1aR activation of ERK1/2. The present study demonstrates that oxytocin can activate different signaling pathways to cause vasorelaxation or vasoconstriction. Oxytocin stimulation of PI3K/eNOS-derived nitric oxide may participate in maintenance of cardiovascular homeostasis, and different vascular reactivities to low or high dose of oxytocin suggest that oxytocin may have different regulatory effects on vascular tone under physiological or pathophysiological conditions.

• Journal of Korean Neurosurgical Society
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• 제56권5호
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• pp.419-422
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• 2014

Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by sudden-onset headache with focal neurologic deficit and prolonged but reversible multifocal narrowing of the distal cerebral arteries. Stroke, either hemorrhagic or ischemic, is a relatively frequent presentation in RCVS, but progressive manifestations of subarachnoid hemorrhage, intracerebral hemorrhage, cerebral infarction in a patient is seldom described. We report a rare case of a 56-year-old woman with reversible cerebral vasoconstriction syndrome consecutively presenting as cortical subarachnoid hemorrhage, intracerebral hemorrhage, and cerebral infarction. When she complained of severe headache with subtle cortical subarachnoid hemorrhage, her angiography was non-specific. But, computed tomographic angiography showed typical angiographic features of this syndrome after four days. Day 12, she suffered mental deterioration and hemiplegia due to contralateral intracerebral hematoma, and she was surgically treated. For recurrent attacks of headache, medical management with calcium channel blockers has been instituted. Normalized angiographic features were documented after 8 weeks. Reversible cerebral vasoconstriction syndrome should be considered as differential diagnosis of non-aneurysmal subarachnoid hemorrhage, and repeated angiography is recommended for the diagnosis of this under-recognized syndrome.

• 대한영상의학회지
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• 제81권5호
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• pp.1239-1245
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• 2020

가역성 대뇌 혈관 수축 증후군(reversible cerebral vasoconstriction syndrome)은 벼락두통과 함께 3개월 안에 소실되는 뇌혈관의 다발성 협착을 특징으로 하는 임상적 영상의학적 증후군이다. 해당 환자 중 일부에서 혈관 벽 조영증강이 보고되고 있으나 그 병태생리학적 의미와 진단적 가치는 불분명하다. 이에 혈관 벽 조영증강을 동반한 가역성 대뇌 혈관 수축 증후군의 증례를 보고하고 병태생리학적 의미와 진단적 가치를 고찰하고자 한다.

• BMB Reports
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• 제51권12호
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• pp.611-612
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• 2018

$C1q/TNF-{\alpha}-Related$ Protein 1 (CTRP1) has recently been shown to act as a blood pressure regulator, as it induces vasoconstriction. In the aorta, CTRP1 facilitates recruitment of angiotensin II receptor 1 (AT1R) to plasma membrane, through activation of the AKT/AS160 signaling pathway. This leads to activation of the Ras homolog gene family (Rho)/Rho kinase (ROCK) signaling pathway, resulting in vasoconstriction. Accordingly, mice overexpressing Ctrp1 have hypertensive phenotype. Patients with hypertension also display higher circulating CTRP1 levels, compared to healthy individuals, indicating that excessive CTRP1 may affect development of hypertension. Conversely, CTRP1 is regarded as an 'innate blood pressure modulator' because CTRP1 increases blood pressure under dehydration to prevent hypotension. Mice lacking Ctrp1 fail to maintain normotension under dehydration conditions, resulting in hypotension, suggesting that CTRP1 is an essential protein for maintaining blood pressure homeostasis. In conclusion, CTRP1 is a novel, anti-hypotensive vasoconstrictor that increases blood pressure during dehydration-induced hypotension.

• Annals of Clinical Neurophysiology
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• 제24권2호
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• pp.68-72
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• 2022

Posterior reversible encephalopathy syndrome (PRES) and reversible cerebral vasoconstriction syndrome (RCVS) are relatively uncommon neurological disorders. These two independent syndromes can be concurrent as a part of a continuum process; however, the specific mechanism is not well known. Although the relationship between RCVS and PRES is currently unclear, they could share a common pathophysiology. This case report aimed to determine the pathophysiology underlying the co-occurrence of PRES and RCVS in a patient with an acute exacerbation of chronic obstructive pulmonary disease.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.164.2-165
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• 2003

Chronic exposure of arsenic is well known to be the cause of cardiovascular disease such as hypertension. In order to investigate the effect of arsenic on blood vessels. we examined whether arsenic affected agonist-induced contraction of aortic rings in isolated organ bath system. Treatment with arsenite increased vasoconstriction induced by phenylephrine or serotonin in a concentration-dependent manner. (omitted)

• 대한영상의학회지
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• 제82권1호
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• pp.261-266
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• 2021

가역적 뇌혈관 수축 증후군은 허혈성 뇌졸중을 야기할 수 있으며 다양한 질환이 원인이 된다. 하지만 빈혈과 가역적 뇌혈관 수축 증후군의 연관성을 나타내는 사례 보고는 거의 없다. 이에 저자들은 보존적 치료로 호전된 66세 여성의 허혈성 뇌졸중과 뇌혈관 수축을 동반한 중증 철결핍빈혈의 사례를 보고하고자 한다. 고해상도 혈관벽 자기공명영상 소견 및 뇌혈관 협착의 가역성을 토대로 가역적 뇌혈관 수축 증후군을 진단할 수 있었다. 가역적 뇌혈관 수축 증후군 및 허혈성 뇌졸중을 가진 환자에서 철결핍빈혈은 하나의 원인으로 고려되어야 하며 즉각적인 처치를 통해 질병의 진행 및 재발을 방지해야 한다.

• Biomolecules & Therapeutics
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• 제24권5호
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• pp.523-528
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• 2016

Urotensin II (UII) is a potent vasoactive peptide and mitogenic agent to induce proliferation of various cells including vascular smooth muscle cells (VSMCs). In this study, we examined the effects of a novel UII receptor (UT) antagonist, KR-36676, on vasoconstriction of aorta and proliferation of aortic SMCs. In rat aorta, UII-induced vasoconstriction was significantly inhibited by KR-36676 in a concentration-dependent manner. In primary human aortic SMCs (hAoSMCs), UII-induced cell proliferation was significantly inhibited by KR-36676 in a concentration-dependent manner. In addition, KR-36676 decreased UII-induced phosphorylation of ERK, and UII-induced cell proliferation was also significantly inhibited by a known ERK inhibitor U0126. In mouse carotid ligation model, intimal thickening of carotid artery was dramatically suppressed by oral treatment with KR-36676 (30 mg/kg/day) for 4 weeks compared to vehicle-treated group. From these results, it is indicated that KR-36676 suppress UII-induced proliferation of VSMCs at least partially through inhibition of ERK activation, and that it also attenuates UII-induced vasoconstriction and vascular neointima formation. Our study suggest that KR-36676 may be an attractive candidate for the pharmacological management of vascular dysfunction.

• 약학회지
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• 제55권2호
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• pp.138-144
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• 2011

The aim of present study was to investigate the possible influence and related mechanism of resveratrol on U-46619 (high concentration)-induced vasoconstriction. Agonist-induced vascular smooth muscle contractions involve the activation of thick or thin filament pathway. However, there are no reports addressing the question whether this pathway is involved in resveratrol-induced relaxation in rat aortae contracted with high U-46619. We hypothesized that MEK or Rho-kinase inhibition plays a role in vascular relaxation evoked by resveratrol in rat aortae. Endothelium-denuded arterial rings from male Sprague-Dawley rats were used and isometric contractions were recorded using a computerized data acquisition system. Resveratrol fully inhibited U-46619 in low concentration-induced contraction regardless of endothelial function. However, resveratrol partially decreased U-46619 in high concentration-induced contraction regardless of endothelial function. Interestingly, only in U-46619 (high concentration)-induced contraction, no significant decrease was observed in phospho-ERK1/2 levels and slight decrease in phospho-MYPT1 levels suggesting that additional pathways different from them or endothelial nitric oxide synthesis might be involved in the vasorelaxation. In conclusion, in high U-46619-contracted rat aortae, resveratrol showed relaxation response regardless of endothelial function significantly but slightly decreasing MYPT1 phosphorylation rather than ERK1/2 phosphorylation.

• Maxillofacial Plastic and Reconstructive Surgery
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• 제32권3호
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• pp.251-255
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• 2010

A local anesthetic agent which is most commonly used for outpatients is lidocaine hydrochloride that contains epinephrine, which is for vasoconstriction in 1:100,000 concentration. This agent is known as a safe local anesthetic agent and has been used widely for topical use or injections. However, the allergic reaction that we will report in this case occurred when common local anesthesia was done intraorally, and the patient complained of hyperventilation, tachycardia, abdominal pain and unintentional tears. We experienced an allergic reaction after injecting the lidocaine hydrochloride and therefore report the case to suggest that local anesthesia should be always carried out very carefully.