• 대한의용생체공학회:의공학회지
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• 제12권3호
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• pp.165-170
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• 1991

Many experiments about endothelial cell seeding on artificial vessels were studied and conducted For this one or a combination of the extramatrix was used for the underlying matrix. But we used the whole ECM(extracellular matrix) that made excreated from flbroblasl. In thls study, we obtained human adult omental microvascular endothelium by collagenase digestion and used polyurthane sheets in order to make a new artificial vessel material. We cultured fibroblast on the polyurethane and gelatin - coated polyurethane. After confluent ingrowth we treated the polyure thane with triton in order to destroy the cytoskeleton and nucleus. We observed the preformed extra cellular matrix on the ployurethane and cultured the isolated microvascular endothelium. We also ok served the growth of microvascular endothelium on the polyurethane and gelatin. We conclude that the use of the whole ECM is promising fair as a new underying substrate for endothelial cell seeding on artificial vessels.

• 약학회지
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• 제43권6호
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• pp.843-850
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• 1999

We investigated whether endothelium-derived NO and endothelin-1 might result enhanced vasoconstriction induced by administration of norepinephrien (NE) at the early stage of one-kidney, one-clip (1K1C) renal hypertensive rats. We also studied the relation ship of renin-angiotensin system (RAS) using rat aorta in this hypothesis. L-NMMA (30$\mu$M) and L-NAME(30${\mu}M$) enhanced vasoconstriction induced by NE in thoracic aorta of control rats. However angiotensin converting enzyme (ACE) inhibitor didn't. The aorta of 1KIC rats showed a singnificantly exaggerated contractile response to NE as compared with control rats. Rub-bing the endothelium abolished this difference. Ach and SNP-induced vasorelaxation show no significant difference between 1KIC and control rats. The treatment of phosphoramidon (10${\mu}M$) and oral administration of captopril (0.05, w/v%) abolished the exaggerated contractile response to NE at early stage of 1KIC rats. These results suggest that the increase of contractile response at the early phase in 1KIC rat is partially involved in the activation of ACE.

• 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.

• 대한한방내과학회지
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• 제24권2호
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• pp.260-268
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• 2003

Object : This study was undertaken to define the mechanism of GwakHyangJungGiSan-induced relaxation in rabbit common carotid artery contracted by agonists. Method : In order to investigate the effect of GwakHyangJungGiSan on rabbit's contracted vascular ring detached from common carotid artery, vascular ring intact or damaged endothelium was used for the experiment using organ bath. To analyze the mechanism of GwakHyangJungGiSan-induced relaxation, GwakHyangJungGiSan extract was infused into contracted vascular ring which had been pretreated by pretreatment of indomethacin(IM), tetraethylammonium chloride(TEA), $N{\omega}-nitro-L-arginine(L-NNA)$. Result : GwakHyangJungGiSan blocks an inflow of $Ca^{2+}$ and relaxes vascular ring by the action of Nitric oxide from endothelium. Consequently when GwakHyangJungGiSan is prescribed, a rise in blood pressure by the resistance of peripheral vessel may be controlled to some extent and so it is anticipated that hypertension, a disorder of blood flow from the vascular contraction and vascular disease will be treated well.

• The Korean Journal of Physiology
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• 제29권2호
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• pp.279-289
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• 1995

This study was designed 1) to develop a hypertensive animal model in which the blood pressures (BPs) of symmetric regions (right and left upper extremities) are significantly different and 2) to test the effect of BP per se on the contractility and endothelium-dependent relaxation of vascular smooth muscle. Rabbits were anesthetized with sodium pentobarbital and ventilated with room air via animal respirator. The transverse aorta was exposed through the left second intercostal space and the lumen of the aorta was narrowed partially by ligation using 3-0 silk and a probe at a point between the origins of the brachiocephalic trunk and the left subclavian artery. Four to eight weeks postoperatively, BPs were measured in the carotid artery as the high BP area (proximal to coactation site) and in the femoral artery as the low BP area (distal to coarctation site). In the animal model, pressure-overload hypertension was developed and the BP of the right subclavian artery was higher than that of the left subclavian artery. The concentrations of circulating epinephrine, norepinephrine, angiotensin I, and angiotensin II were measured. The right and left subclavian arteries and their branches were used for isometric tension recording in organ baths and their responsiveness to phenylephrine, serotonin, acetylcholine, and sodium nitroprusside were examined. The BPs of carotid and femoral artery in control animals were $116{\pm} 12/75{\pm}9\;mmHg (mean ${\pm}SEM$) and $130{\pm}16/68{\pm}9\;mmHg$ respectively, while those of carotid and femoral artery in the hypetensive animals were $172{\pm}6/111{\pm}10\;mmHg$ and 136{\pm} 4/100 {\pm}9\;mmHg$ respectively. There were no significant differences in the concentrations of circulating epinephrine, norepinephrine, angiotensin I, and angiotensin II between controls and the animal models. No significant differences were found in the vascular sensitivities to phenylephrine and serotonin between the high pressure-exposed vessels and the low pressure-exposed vessels. However, the endothelium-dependent relaxation to acetylcholine and nitroprusside-induced relaxation showed significant differences between the high pressure-exposed and the low pressure-exposed subclavian arteries. From the above results, we suggest that the contractility of vascular smooth muscle is unchanged by the elevated pressure per se. However, the endothelium-dependent relaxation to acetylcholine and the nitroprusside-induced relaxation are attenuated by pressure.

• The Korean Journal of Physiology and Pharmacology
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• 제4권6호
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• pp.471-477
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• 2000

In the rabbit renal artery, acetylcholine $(ACh,\;1\;nM{\sim}10\;{\mu}M)$ induced endothelium-dependent relaxation of arterial rings precontracted with norepinephrine $(NE,\;1\;{\mu}M)$ in a dose-dependent manner. $N^G-nitro- L-arginine$ (L-NAME, 0.1 mM), an inhibitor of NO synthase, or ODQ $(1\;{\mu}M),$ a soluble guanylate cyclase inhibitor, partially inhibited the ACh-induced endothelium-dependent relaxation. The ACh-induced relaxation was abolished in the presence of 25 mM KCl and L-NAME. The cytochrome P450 inhibitors, 7- ethoxyresorufin $(7-ER,\;10\;{\mu}M),$ miconazole $(10\;{\mu}M),$ or 17-octadecynoic acid $(17-ODYA,\;10\;{\mu}M),$ failed to inhibit the ACh-induced relaxation in the presence of L-NAME. 11,12-epoxyeicosatrienoic acid $(11,12-EET,\;10\;{\mu}M)$ had no relaxant effect. The ACh-induced relaxation observed in the presence of L-NAME was significantly reduced by a combination of iberiotoxin $(0.3\;{\mu}M)$ and apamin $(1\;{\mu}M),$ and almost completely blocked by 4-aminopyridine (5 mM). The ACh-induced relaxation was antagonized by $P_{2Y}$ receptor antagonist, cibacron blue $(10\;and\;100\;{\mu}M),$ in a dose-dependent manner. Furthermore, 2-methylthio-ATP (2MeSATP), a potent $P_{2Y}$ agonist, induced the endothelium-dependent relaxation, and this relaxation was markedly reduced by either the combination of iberiotoxin and apamin or by cibacron blue. In conclusion, in renal arteries isolated from rabbit, ACh produced non-NO relaxation that is mediated by an EDHF. The results also suggest that ACh may activate the release of ATP from endothelial cells, which in turn activates $P_{2Y}$ receptor on the endothelial cells. Activation of endothelial $P_{2Y}$ receptors induces a release of EDHF resulting in a vasorelaxation via a mechanism that involves activation of both the voltage-gated $K^+$ channels and the $Ca^{2+}-activated\;K^+\;channels$. The results further suggest that EDHF does not appear to be a cytochrome P450 metabolite.

• 동의생리병리학회지
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• 제29권6호
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• pp.492-497
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• 2015

In the present study, vasorelaxant effect of the extract of seeds of Oenothera odorata (SOO) and its possible mechanism responsible for this effect were examined in vascular tissues isolated from rats. Changes in vascular tension, 3',5'-cyclic monophosphate (cGMP) levels were measured in thoracic aorta rings from rats. Methanol extract of seeds of Oenothera odorata relaxed endothelium-intact thoracic aorta in a dose-dependent manner. A dose-dependent vascular relaxation was also revealed by treatment of ethylacetate, n-butanol, and H₂O (aqua extract of seeds of Oenothera odorata , ASOO) extracts partitioned from methanol, but not by hexane extract. However, the vascular relaxation induced by ASOO were abolished by removal of endothelium of aortic tissues. Pretreatment of the endothelium-intact vascular tissues with N^G-nitro-L-arginine methyl ester (L-NAME) or ¹H-[1,2,4]-oxadiazole-[4,3-α]-quinoxalin-1- one (ODQ) significantly inhibited vascular relaxation induced by ASOO. Moreover, incubation of endothelium-intact aortic rings with ASOO increased the production of cGMP. However, ASOO-induced increases in cGMP production were blocked by pretreatment with L-NAME or ODQ. The vasorelaxant effect of ASOO was attenuated by tetraethylammonium (TEA), 4-aminopyridine, and glibenclamide attenuated. On the other hand, the ASOO-induced vasorelaxation was not blocked by verapamil, and diltiazem. Taken together, the present study demonstrates that ASOO dilate vascular smooth muscle via endothelium-dependent NO-cGMP signaling pathway, which may be closely related with the function of K⁺ channels.

• 동의생리병리학회지
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• 제21권2호
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• pp.408-413
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• 2007

Vascular tone plays an important role in the regulation of blood pressure. In the present study, the methanol extract of Rosae multiflora Radix (MRM) induced dose-dependent 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 methly ester (L-NAME) or 1H-[1,2,4]-oxadiazole-[4,3-${\alpha}$]-quinoxalin-1-one (ODQ) inhibited the relaxation induced by MRM, respectively. But, the relaxation effect of MRM was not blocked by indomethacine, glibenclamide, tetraethylammonium (TEA), verapamil, diltiazem, atropine, and propranolol, respectively. Moreover, incubation of endothelium-intact aortic rings with MRM increased the production of cGMP. Taken together, the present results suggest that MRM relaxes vascular smooth muscle via endothelium-dependent nitric oxide/cGMP signaling. These results would be useful for further study to MRM on animal models with cardiovascular diseases.

• Journal of Ginseng Research
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• 제34권4호
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• pp.314-320
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• 2010

The previous reports have showed that ginseng saponins, which are the active ingredients of Panax ginseng, cause the relaxation of artery that are contracted due to a various of hormones or potassium ($K^+$). Recently, we also showed that ginsenosides differentially regulate channel activity. The purpose of this study was to examine whether ginseng saponins affect contraction induced by $K^+$, serotonin (5-HT), or acetylcholine (Ach) in porcine coronary vessel. Treatment with concentrations of ginseng saponins caused a relaxation of 25 mM KCl-induced porcine coronary artery contraction. Also, ginseng saponin induced a significant dose-dependent relaxation of $3\;{\mu}M$ 5-HT-induced porcine coronary artery with the endothelium. In the porcine artery with the endothelium, ginseng saponins induced a relaxation by $3\;{\mu}M$ 5-HT in a concentration-dependent pattern. Ginseng saponins induced relaxation of both 25 mM KCl- and $3\;{\mu}M$ 5-HT-induced coronary artery contraction in the absence and presence of the endothelium. In contrast, treatment with $100\;{\mu}g/mL$ ginseng saponin did not induce relaxation in coronary artery contraction induced by Ach ($0.01\;{\mu}M$ to $30\;{\mu}M$) in the presence of the endothelium, but did cause significant relaxation of coronary artery contractions by Ach ($0.01\;{\mu}M$ to $30\;{\mu}M$) in the absence of the endothelium. These findings indicate that ginseng saponin (> $100\;{\mu}g/mL$) significantly inhibits porcine coronary artery contractions caused by $K^+$, 5-HT, and Ach. Therefore, in this study, we demonstrated that ginseng saponin may show beneficial roles on abnormal coronary contraction.

• The Korean Journal of Physiology and Pharmacology
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• 제21권6호
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• pp.591-598
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• 2017

Propofol is known to cause vasorelaxation of several systemic vascular beds. However, its effect on the pulmonary vasculature remains controversial. In the present study, we investigated the effects of propofol on human pulmonary arteries obtained from patients who had undergone surgery. Arterial rings were mounted in a Multi-Myograph system for measurement of isometric forces. U46619 was used to induce sustained contraction of the intrapulmonary arteries, and propofol was then applied (in increments from $10-300{\mu}m$). Arteries denuded of endothelium, preincubated or not with indomethacin, were used to investigate the effects of propofol on isolated arteries. Propofol exhibited a bifunctional effect on isolated human pulmonary arteries contracted by U46619, evoking constriction at low concentrations ($10-100{\mu}m$) followed by secondary relaxation (at $100-300{\mu}m$). The extent of constriction induced by propofol was higher in an endothelium-denuded group than in an endothelium-intact group. Preincubation with indomethacin abolished constriction and potentiated relaxation. The maximal relaxation was greater in the endothelium-intact than the endothelium-denuded group. Propofol also suppressed $CaCl_2$-induced constriction in the 60 mM $K^+$-containing $Ca^{2+}$-free solution in a dose-dependent manner. Fluorescent imaging of $Ca^{2+}$ using fluo-4 showed that a 10 min incubation with propofol ($10-300{\mu}m$) inhibited the $Ca^{2+}$ influx into human pulmonary arterial smooth muscle cells induced by a 60 mM $K^+$-containing $Ca^{2+}$-free solution. In conclusion, propofol-induced arterial constriction appears to involve prostaglandin production by cyclooxygenase in pulmonary artery smooth muscle cells and the relaxation depends in part on endothelial function, principally on the inhibition of calcium influx through L-type voltage-operated calcium channels.