• 약학회지
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• 제56권3호
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• pp.180-185
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• 2012

The aim of present study was to investigate the possible influence and related mechanism of alcohol on the arterial contraction. Vascular contraction involves the activation of thick or thin filament pathway. However, there are no reports addressing the question whether this pathway is involved in alcohol-induced regulation. We hypothesized that alcohol plays a role in vascular contraction evoked by a vasoconstrictor in rat aortae regardless of endothelial function. Denuded arterial rings from male rats were used and isometric contractions were recorded using a computerized data acquisition system. Interestingly, alcohol at a low concentration (3% v/v) inhibited thromboxane $A_2$ or phorbol ester-induced contraction with endothelial function but at a high concentration (10%) didn't inhibit and rather increased the contraction in the denuded muscle. Therefore, alcohol at a low concentration decreases the contraction and alcohol at a high concentration increases the contraction suggesting that additional pathways different from endothelial nitric oxide synthesis might be involved in the regulation of contractility. In conclusion, alcohol has some effect on the regulation of contractility regardless of endothelial function.

• 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)

• 한국독성학회:학술대회논문집
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• 한국독성학회 2002년도 Molecular and Cellular Response to Toxic Substances
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• pp.156-156
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• 2002

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.(omitted)

• Journal of Chest Surgery
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• 제39권12호
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• pp.943-945
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• 2006

수유 곤란과 반복적인 흡인성 폐렴을 주소로 내원한 11개월 된 여아가 우대동맥궁, Kommerell 게실, 식도 후방의 좌쇄골하 및 동맥관 인대로 형성된 완전 혈관륜을 진단 받고 수술적 교정을 받았다. 수술은 좌측 후측 개흉 후 동맥관 인대를 분리하여 식도 압박 요인을 제거하고, Kommerell 게실을 하행대동맥으로부터 분리, 절제한 후 좌쇄골하 동맥을 좌측 총경동맥으로 단측 문합하였다. 환아의 수술 경과는 양호하였으며, 현재 외래 관찰 중이다.

• 약학회지
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• 제50권4호
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• pp.293-299
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• 2006

The aim of present study was to investigate the possible influence of Rho-kinase inhibition on the plant-derived estrogen-like compounds-induced arterial relaxation. Agonist- or depolarization-induced vascular smooth muscle contractions involve the activation of Rho-kinase pathway. However there are no reports addressing the question whether this pathway is involved in genistein-or daidzein-induced vascular relaxation in rat aortae precontracted with phenylephrine or thromboxane $A_2$ mimetic U-46619. We hypothesized that Rho-kinase inhibition plays a role in vascular relaxation evoked by genistein or daidzein in rat aortae. Endothelium-intact and denuded arterial rings from male Sprague-Dawley rats were used and isometric contractions were recorded using a computerized data acquisition system. Genistein concentration-dependently inhibited phenylephrine or thromboxane $A_2-induced$ contraction regardless of endothelial function. Surprisingly, in the agonists-induced contraction, similar results were also observed in aortae treated with daidzein, the inactive congener for protein tyrosine kinase inhibition, suggesting that Rho-kinase might act upstream of tyrosine kinases in phenylephrine-induced contraction. In conclusion, in the agonists-precontracted rat aortae, genistein and daidzein showed similar relaxant response regardless of tyrosine kinase inhibition or endothelial function.

• 생약학회지
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• 제37권2호통권145호
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• pp.67-73
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• 2006

The butanol extracts of Agrimonia pilosa (BAP) induced dose-dependent vascular relaxation of phenylephrine-precontracted aorta, which was abolished by removal of functional endothelium. Pretreatment of the endothelium-intact aortic tissues with $N^G$-nitro-L-arginine methyl ester (L-NAME) and 1H-[1,2,4]-oxadiazole-[$4,3-{\alpha}$]-quinoxalin-1-one(ODQ) inhibited the relaxation induced by BAP. BAP-induced vascular relaxation was also markedly attenuated by addition of verapamiI, while the relaxant effect of BAP was not blocked by indomethacine, glibenclamide, tetraethylammonium (TEA), atropine, or propranolo. In addition, incubation of endothelium-intact aortic rings with BAP increased the vascular production of cGMP. These results suggest that BAP relaxes vascular smooth muscle via endothelium-dependent nitric oxide/cGMP signaling pathway, which may be causally related with L-type $Ca^{2+}$ channels.

• Biomolecules & Therapeutics
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• 제26권2호
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• pp.139-145
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• 2018

The present study was undertaken to investigate the influence of hypothermia on endothelium-independent vascular smooth muscle contractility and to determine the mechanism underlying the relaxation. Denuded aortic rings from male rats were used and isometric contractions were recorded and combined with molecular experiments. Hypothermia significantly inhibited fluoride-, thromboxane $A_{2-}$, phenylephrine-, and phorbol ester-induced vascular contractions regardless of endothelial nitric oxide synthesis, suggesting that another pathway had a direct effect on vascular smooth muscle. Hypothermia significantly inhibited the fluoride-induced increase in pMYPT1 level and phorbol ester-induced increase in pERK1/2 level, suggesting inhibition of Rho-kinase and MEK activity and subsequent phosphorylation of MYPT1 and ERK1/2. These results suggest that the relaxing effect of moderate hypothermia on agonist-induced vascular contraction regardless of endothelial function involves inhibition of Rho-kinase and MEK activities.

• 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.

• The Korean Journal of Physiology
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• 제29권1호
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• pp.39-50
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• 1995

This study was designed to clarify the action of cyclic nucleotides, cyclic AMP and cyclic GMP, on phorbol 12,13-dibutyrate (PDBu)-induced contraction in rings isolated from rabbit carotid artery. Arterial rings, 2 mm in width, were myographied isometrically in an isolated organ bath. PDBu produced slowly developing, sustained contraction in rabbit carotid artery, in a dose dependent manner, which was independent of extracellular $Ca^{2+}$ PDBu-induced contraction was relaxed by staurosporine, which suggests that PDBu-induced contraction is mediated by protein kinase C (PKC). $^{45}Ca^{2+}$ uptake by rabbit carotid artery was increased by PDBu during depolarization, but not in control. Isoproterenol and sodium nitroprusside (SNP) relaxed phenylephrine-induced contraction. However, SNP but not isoproterenol relaxed the contraction induced by PDBu. Acetylcholine relaxed PDBu-induced contraction in the presence of the endothelium. 8-bromo-cyclic AMP, a permeable analogue of cyclic AMP, suppressed phenylephrine-induced contraction but not PDBu-induced contraction. 8-bromo cyclic GMP relaxed both of them with dose dependency. A large dose of forskolin relaxed PDBu-induced contraction. PDBu increased cyclic AMP without considerable change in the level of cyclic GMP. Based on these findings, PDBu-induced contraction of rabbit carotid artery was relaxed by cyclic GMP more effectively than cyclic AMP, and the action of cyclic AMP could be mediated by cyclic GMP dependent protein kinase. Therefore it is suggested that the antagonistic action between protein kinase C and cyclic GMP-dependent protein kinase plays a major role in the regulation of vascular tone.

• Journal of Chest Surgery
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• 제42권5호
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• pp.576-587
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• 2009

배경: Nitric oxide (NO)-cGMP 신호전달체계의 상향 조절(up-regulation)이 급성심근경색 3일 후 흰쥐의 혈관반응성의 변화에 관여한다고 알려져 있으나 그 기전에 대해서는 명확히 규명되지 않았다. 대상 및 방법: 좌전하행관상동맥을 30분간 폐쇄한 후 급성심근경색을 유도한 군을 AMI군으로, 동일한 모의 수술(sham operation)을 하였으나 관상동맥을 폐쇄하지 않은 군을 SHAM군으로 하였다 AMI 혹은 SHAM수술 3일 후 흰쥐의 대동맥 고리절편(내피를 보존한 대동맥 절편을 E(+), 내피를 제거한 대동맥 절편을 E(-))에서 phenylephrine (PE), KCl, acetylcholine (Ach) 및 sodium nitroprusside (SNP)에 대한 농도-반응 관계를 측정하였다 AMI군의 E(+) 대동맥 절편에서 PE의 농도-반응 관계를 NO synthase (NOS) 억제제인 $N{\omega}$-nitro-L-arginine methyl ester (L-NAME)와 cyclooxygenase 억제제인 indomethacin으로 각각 전처치한 대동맥 절편과 비교하였다. 혈장 nitrite/nitrate 농도는 Griess reaction으로 측정하였고, 방사면역 분석법을 이용한 흉부 대동맥 절편의 cGMP정량과 real time PCR을 이용한 endothelial nitric oxide synthase (eNOS) mRNA 발현양상 측정을 하였다. 결과: AMI군에서의 심근경색의 평균 크기는 $21.3{\pm}0.62%$였다. AMI군에서 심박수와 수축기 및 이완기 혈압은 의미있는 변화가 없었다. E(+)와 E(-) 대동맥 절편에서 PE와 KCl에 대한 수축반응의 민감도는 AMI군 대동맥 절편에서 의미 있게 감소하였다(p<0.05). L-NAME은 이러한 수축반응을 완전하게 역전시켰으나 indomethacin은 효과가 없었다(p<0.05). 또한 AMI군에서 Ach에 대한 이완반응의 민감도가 의미 있게 감소하였다(p<0.05). AMI군에서 SHAM군에 비해 혈장 nitrite/nitrate 농도(p<0.05), 기저 cGMP 농도(p<0.05), 및 eNOS mRNA 발현양상(p=0.056)이 증가하였다. 결론: 이상의 결과들로 보아 eNOS의 발현 증가와 NO-cGMP 신호전달체계의 상향조절이 급성심근경색 3일 후 흰쥐 흉부대동맥에서의 수축 및 이완 반응성 감소의 원인으로 생각된다.