• Journal of Environmental Science International
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• v.12 no.10
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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.

• Journal of Environmental Science International
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• v.12 no.6
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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.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.4
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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.

• The Journal of Korean Medicine
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• v.24 no.4
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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.

• YAKHAK HOEJI
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• v.37 no.2
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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.

• The Korean Journal of Pharmacology
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• v.32 no.1
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• pp.51-56
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• 1996

The objectives of this study is to find out mechanism of vasodilating effects of ANP in 2K-1C renovascular hypertensive rat aorta and to compare with those of normotensive rat aorta. In 2K-1C renovascular hypertensive rat, average arterial blood pressure and plasma renin activity were higher than in normotensive rat. In 2K-1C renovascular hypertensive rat aorta, NE sensitivity was more increased and maximal contraction of aorta by NE was higher than those of normotensive rat aorta. ANP inhibited NE-induced contraction in both 2K-1C renovascular hypertensive and normotensive rat aorta, concentration-dependently. However, ANP was less effective for relaxing NE-induced contraction in 2K-1C renovascular hypertensive rat aorta than in normotensive rat aorta. ANP inhibited $^{45}Ca^{2+}$ uptake induced by NE in both 2K-1C renovascular hypertensive and normotensive rat aorta. From these results. inhibition of $Ca^{2+}$ influx may be one of the vasodilating mechanism of ANP in 2K-1C renovascular hypertensive rat aorta. Although the potency of ANP in relaxing NE-induced contractions was attenuated, the efficacy of ANP was not changed in 2K-1C renovascular hypertensive rat aorta compared with that of ANP in normotensive rat aorta. Abbreviations: ANP, Atrial natriuretic peptide; 2K-1C, 2-kidney 1 clip; NE, norepinephrine; SHR, Spontaneously hypertensive rat; DOC, Deoxycorticosterone; EDTA, Ethylenediaminetetra-acetic acid; PSS, Physiological salt solution; TRIS, tris(hydroxymethyl) aminomethane

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.4
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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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• v.19 no.6
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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.

• Korean Journal of Environmental Biology
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• v.21 no.3
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• pp.313-318
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• 2003

Environmental stresses, such as heat shock, alcohol and physiological salt have been shown to induce a group of protein called heat shock protein (HSPs) in various tissues. In this investigation, we studied that arsenic stress would alter contraction of isolated rat aorta and expression of heat shock protein 70 and investigated the relation between expression of HSP 70 and vascular contractility of isolated rat aorta. Rat aorta strips, mounted in organ baths were exposed to 0, 0.5, 1,2 and 4 mM arsonic for 60 min. and 1,3 and 8 hours later tested for contractile response and expression of heat shock protein 70. Contractility of rat aorta were determined by isometric transducer connected to computerized physiograph and expression of HSP 70 was characterized by western blotting, respectively. Potassium chloride (55 mM) significantly augmented vascular contractility of yat aorta by 39％ compared with the control at 8 hours but not one or three hours after treatment of 4 mM arsenic. Arsonic stress (4 mM) also increased the expression of HSP 70 in rat aorta at 8 hours but one or three hours compared with the control and HSP expressed in vascular smooth muscle cells and some expressed in endothelium cells. These results suggest that arsenic stress not only did alter the magnitude of the contractile response to high potassium chloride but also increased the expression of HSP 70 in the rat aorta.

• Biomolecules & Therapeutics
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• v.9 no.2
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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.