• 한국환경과학회지
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• 제12권10호
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• pp.1131-1136
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• 2003

To examine whether salt stress would alter or not contractility of isolated rat aorta, under anesthesia with sodium pentobarbital(50 mg kg-1 i.p.), male Sprague Dawley rats(300-330 g) were subjected to 0, 50, and 150 mM of sodium chloride at 37$^{\circ}C$ for 60 min. where as the sham group was left at modified Krebs-bicarbonate solution. To measure contractile response of vascular ring preparation isolated from rat was determined in organ bath and was recorded on physiograph connected to isometric transducer. And the strip was checked for expression of heat shock protein(Hsp) by Western blotting. One, three and eight hours later, we measured vascular contractility of isolated rat aorta treated with KCI, phenylephrine from organ bath study. The dose-vascular responses of potassium chloride and phenylephrine showed a little augmentation by NaCl concentration in the strips exposed to NaCl for 8 hours. And the response of relaxation induced by nitroprusside and acetylcholine was not influenced by NaCl stress in isolated aorta ring for 8 hours, respectively. Expression pattern of Hsp 70 of vascular muscle in isolated rat aorta showed a little increase in 150 mM NaCl group at 8 hours after NaCl treatment but not at 3 hours, and Hsp 60 expression of rat aorta was markedly increased in 50 mM NaCl group at 8 hours after NaCl treatment. Taken together, NaCl induced dose-and time dependent accumulation of the Hsp but not affected contraction of rat aorta. These data suggest that short term high salt stress was not sufficient to induce hypertension of rat aorta.

• 한국환경과학회지
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• 제12권6호
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• pp.651-657
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• 2003

In order to examine if arsenic, one of environmental stresses, contributes to hypertension as one of cardiovas cular pathological factors, this study was perfarmed in vivo and in vitro, using intacted or pithed rats and aorta ring preparation, respectively. And also the relationship between expression of heat shock protein (HSP) 90 and vasoactives-induced contractile response was elucidated. To measure blood pressure, the carotid arterial pressure was recorded on physiograph(Grass Co. 79E) connected to strain gauge. On the other hand, contractile response of vascular ring preparation isolated from rat was determined in organ bath and was recorded on physiograph connected to isometric transducer. And HSP was detacted by Western blotting whole cell Iysis. Preganglionic nerve stimulation was increased by 26.0% in arterial pressure of rat treated with arsenic. Vascular contractile response was monitored and HSP were measured by Western blotting of whole Iysis prepared from samples exposed with 0, 0.5, 1, 2 and 4 mM of arsenic for 8 hours. The dose-vascular responses of potassium chloride were augmented by increasing dose of arsenic in the strips exposed to arsenic for 8 hours, and were not augmented for 1, 3, 5 hours. And the response of relaxation of rat aorta induced by histamine was not influenced by arsenic stress. The increase of HSP 90 expression in rat aorta was pronounced at 8 hours after 4 mM of arsenic treatment, but HSP 60 expression was not. Arsenic stress not only increased the expression of HSP 90 in the rat aorta, but also augmented contractions to potassium chloride. These results indicated that arsenic stress was sufficient to induce heat shock protein 90, resulting in increased vascular contractility in rat aorta.

• 동의생리병리학회지
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• 제18권4호
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• pp.1107-1110
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• 2004

The purpose of this research was to investigate the effects of supercritical fluid extract of Kamichungbieum (SFE) on the contraction of isolated rat aorta. The contractile force of rat aorta was measured with force displacement transducer under 1.5g loading tension. The contraction of aorta induced by phenylephrine 0.1 μM was inhibited by SFE. The aorta relaxed by SFE was inhibited by the pretreatment of L-NNA, ODQ or indomethacin, respectively. These results indicate that SFE induce the relaxation of isolated aorta via activation of nitric oxide, cAMP and cyclooxygenase in epithelium cells.

• 대한한의학회지
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• 제24권4호
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• pp.87-91
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• 2003

Objectives: To examine the relaxational response to the water extract of Rheum palmatum L. and Rheum undulatum L. on rat thoracic aorta and abdominal aorta. Methods: Segments of thoracic aorta and abdominal aorta obtained from rats immediately after delivery were mounted in organ baths superfused on a polygraph. Results : We found that the thoracic aorta segments responded to the water extract of genus Rheum with a dose-dependent vasorelaxation. At $10^{-4}$ M 5-HT, the maximal contraction force was 93.5% of the maximum KCI-response. The 5-HT induced contractions at $10^{-4}$ M were inhibited by 86.4% and 62.1 % after addition of the high concentrations of R. palmatum root (RPR) and leaf (RPL) and R. undulatum root (RUR) and leaf (RUL). At 10 mg/ml RPR and RUR, the relaxational response at thoracic aorta and abdominal aorta with and without endothelium were 86.4%, 83.2%, 85.8%, and 62.1% of the maximum 5-HT induced contraction. Conclusion: Our result showed that RPL and RUL induced dose-dependent vasorelaxation on rat thoracic aorta and abdominal aorta, and that RPL and RUL roots have more potent effects than the leaves.

• 약학회지
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• 제37권2호
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• pp.163-171
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• 1993

In order to study the functions of vascular endothelial nitric oxide(NO) generating system, we examined the effects of monomethylarginine(MMA) and dimethylarginine(DMA)(asym., sym.), arginine analogues, on modulation of vascular tone. Also, the concentrations of endogenous arginie and MMA were measured by HPLC in rat aortic tissues. The results were as follows. 1. The maximum relaxation induced by Ach (1.5$\times$10$^{-6}$M) was 80% of the contractility of rings of rat aorta induced by phenylephrine and L-Arg causes endothelium-dependent relaxation of the aorta precontracted with phenylephrine and these relaxation were concentration-dependent. 2. Endothelium-dependent contractility of rings of rat aorta induced by MMA (100 $\mu{M}$), DMA (asym., 100 $\mu{M}$) and DMA (sym., 100 $\mu{M}$) were 25.5%, 27.5% and 16.5% of that induced by phenylephrine respectively. 3. The relaxation of rat aortic ring induced by L-Arg was inhibited by MMA, DMA(asym.) and DMA(sym.). The degrees of inhibition induced by MMA, DMA(asym.) and DMA(sym.) were 45.7%, 37.1% and 18.3%, respectively. 4. The endogenous arginine and monomethylarginine contents in rat aorta were 83 pmoles/mg wet tissue, and 34.9 pmoles/mg wet tissue. After stimulation with Ach, the concentrations of L-Arg and MMA were significantly decreased. These results suggest that there are the strong relationships between the endogenous L-Arg and methylated arginines and NO-generating system.

• 대한약리학회지
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• 제32권1호
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• pp.51-56
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• 1996

본 연구의 목적은 2-kidney 1 clip (2K-1C) 신혈관성 고혈압흰쥐에서 심방이뇨펩이드의 혈관 이완작용의 기전을 규명하고 정상혈압흰쥐에서의 혈관이완작용과 비교하는 것이다. 2K-1C 신혈관성 고혈압흰쥐는 정상혈압흰쥐에 비하여 평균동맥압의 유의한 상승과 혈장레닌활성의 증가가 관찰되었다. 2K-1C 신혈관성 고혈압흰쥐의 대동맥에서 norepinephrine (NE)의 수축력의 감수성 및 최대 수축력이 정상혈압흰쥐의 대동맥보다 증가하였다. 심방이뇨펩타이드는 NE에 의한 수축을 농도-의존적으로 각각의 혈압군에서 억제하였다. 그러나, 2K-1C 신혈관성 고혈압흰쥐에서 심방이뇨펩타이드의 NE 억제 작용은 전체적으로 정상혈압흰쥐에서 보다 감소되었다. 그러나 최대 용량의 심방이뇨펩타이드의 NE 이완작용은 양 고혈압군에서 차이가 없었다. 2K-1C 신혈관성 고혈압흰쥐에서 NE에 의하여 $Ca^{2+}$의 유입이 유의하게 증가하였고, 심방이뇨펩타이드는 이 증가를 억제하였다. 정상혈압흰쥐에서도 심방이뇨펩타이드는 NE에 의하여 유의하게 증가된 $Ca^{2+}$의 유입을 억제하였다. 이상과 같은 결과로 볼 때 정상혈압흰쥐와 2K-1C 신혈관성 고혈압흰쥐의 심방이뇨펩타이드의 이완작용의 기전에는 $Ca^{2+}$의 유입 차단이 관여할 것으로 추측되며, 이때 심방이뇨펩타이드의 NE 수축억제에 대한 potency는 2K-1C 신혈관성 고혈압 흰쥐에서 감소하였으나 efficacy는 정상혈압흰쥐와 비교하여 변함이 없음이 관찰되었다.

• The Korean Journal of Physiology and Pharmacology
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• 제27권4호
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• pp.325-331
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• 2023

α₁-adrenoceptors link via the G-protein Gq/G₁₁ to both Ca²⁺ entry and release from stores, but may also activate Rho kinase, which causes calcium sensitization. This study aimed to identify the subtype(s) of α₁-adrenoceptor involved in Rho kinase-mediated responses in both rat aorta and mouse spleen, tissues in which contractions involve multiple subtypes of α₁-adrenoceptor. Tissues were contracted with cumulative concentrations of noradrenaline (NA) in 0.5 log unit increments, before and in the presence of an antagonist or vehicle. Contractions produced by NA in rat aorta are entirely α₁-adrenoceptor mediated as they are competitively blocked by prazosin. The α_1A-adrenoceptor antagonist RS100329 had low potency in rat aorta. The α_1D-adrenoceptor antagonist BMY7378 antagonized contractions in rat aorta in a biphasic manner: low concentrations blocking α_1D-adrenoceptors and high concentrations blocking α_1B-adrenoceptors. The Rho kinase inhibitor fasudil (10 µM) significantly reduced aortic contractions in terms of maximum response, suggesting inhibition of α_1B-adrenoceptor mediated responses. In the mouse spleen, a tissue in which all 3 subtypes of α₁-adrenoceptor are involved in contractions to NA, fasudil (3 µM) significantly reduced both early and late components to the NA contraction, the early component involving α_1B- and α_1D-adrenoceptors, and the late component involving α_1B- and α_1A-adrenoceptors. This suggests that fasudil inhibits α_1B-adrenoceptor mediated responses. It is concluded that α_1D- and α_1B-adrenoceptors interact in rat aorta and α_1D-, α_1A- and α_1B-adrenoceptors interact in the mouse spleen to produce contractions and these interactions suggest that one of the receptors preferentially activates Rho kinase, most likely the α_1B-adrenoceptor.

• Archives of Pharmacal Research
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• 제19권6호
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• pp.462-468
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• 1996

The present study was undertaken to investigate the effects of age on angiotensin II (AII) response and antagonistic activity of losartan using aortic rings and liver homogenates from rats ranging in age from 0.7 to 20 months. Whether the endothelium was present or not, the maximum contractile response to AII decreased with age. Removal of the endothelium enhanced AII-induced maximum contraction and these endothelial effects seemed to be due to endothelium-derived relaxing factor (EDRF) in all ages. Equilibrium binding studies demonstrated an age-related decrease in maximum binding $(B_{max})$ with little change in binding affinity $(K_d)$. In rat aorta, the extent of losartan-induced parallel shifts $(K_B)$ in AII concentration-response curves was not significantly different between ages. In addition, $IC_{50}$ value of losartan in competition binding was not changed with age in rat liver homogenates. These results suggest that the potency of losartan is not altered with age in rat aorta and liver, although AII-induced contractile response and the maximum AII binding decreased significantly with age.

• 환경생물
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• 제21권3호
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• pp.313-318
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• 2003

외부에서 투여된 열자극, 알콜 및 생리적 염과 같은 환경 스트레스는 체내 각 부위에서 스트레스단백질(열자극단백질, HSP)을 생성하게 된다. 본 연구에서는 비소가 흰쥐 대동맥의 수축에 미치는 영향을 조사하기 위해 스트레스단백질의 발현과 대동맥의 수축력의 변화와 이들과의 관계를 알아보고자 실험을 실시하였다 적출한 혈관은 organ bath에 담가 0, 0.5, 1, 2,및 4 mM As를 처리한 후 1, 3, 및 8시간 뒤에 KCI(55 mM)에 대한 수축반응과 HSP 발현을 각각 생리기록계와 western blotting 을 통해 분석하였다. 비소(4 mM)를 처리한 혈관의 KCI에 대한 수축력은 처리 초기(1, 3시간)에는 효과가 없었고 처리 8시간째 대조군에 비해 39％로 유의적인 증가를 보였다. 또한 비소처리로 혈관의 스트레스단백질 HSP 70의 생성은 비소 처리농도에 따라 증가되었고, 비소 처리 초기에는 변화가 없었으며 비소처리 8시간째 HSP생성이 촉진되었다. HSP는 주로 혈관 평활근세포에서 현저하게 발현되었고 일부 내피세포에서도 발현되었다. 이상의 결과에서 비소 처리에 따른 HSP 70의 발현과 혈관의 수축 증가의 상승되는 현상이 비소처리 8시간째에 유의하게 증가되는 것으로 보아, 비소처리에 의해 혈관의 스트레스단백질 HSP 발현이 증가되고 이로 인해 혈관 수축력을 상승시켜 고혈압 유발과정에 관여하는 것으로 여겨진다.

• Biomolecules & Therapeutics
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• 제9권2호
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• pp.119-124
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• 2001

In order to determine the role of dehydroepiandrosterone (DHEA), the important sex-steroid hormone precursor, in vascular reactivity in rats, animals were treated for two weeks with DHEA or sex hormones, and the vascorelaxant and contractile responses of isolated aorta were examined. DHEA diminished the acetylcholine (ACh)-induced relaxation in female rats, while the drug was without effect in males. Testoterone lowered the vasorelaxant activity to ACh in either sex. 17$\beta$-Estradiol enhanced ACh-induced vasorelaxation in male rats, but this female sex hormone did not influence in females. In male rats, the androgen receptor antagonist flutamide also enhanced vasorelaxant action of ACh. When the male rat aorta was incubated in vitro with a nitric oxide (NO) synthase inhibitor L-NAME, phenylephrine-induced contraction was greatly potentiated in DHEA-pretreated rats compared to control ones. The present results suggest that DHEA stimulates mainly androgen in female, but both androgen and estrogen in male rats. The participation of NO In the modulation of vascular reactivity with pretreated DHEA was also considered.