• Advances in Traditional Medicine
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• v.2 no.2
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• pp.87-93
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• 2002

The present study was aimed to examine the role of endothelium in the relaxant effect of hawthorn fruit extract of Crataegus pinnatifida in four different types of rat arteries, posterior cerebral communicating artery, right descending coronary artery, common carotid artery, and aorta. In $9,11-dideoxy-11{\alpha}$, $9{\alpha}-epoxy-methanoprostaglandin$ $F_{2{\alpha}}$ (U46619)-preconstricted arterial rings except for aorta, the extract produced endothelium-independent relaxations with similar potency. This relaxation was unaffected by pretreatment with $100\;{\mu}M\;N^G-nitro-L-arginine$ methylester (L-NAME, the nitric oxide synthase inhibitor), $3\;{\mu}M$ 1H-[l,2,4]oxadiazolo$[4,2-{\alpha}]$quinoxalin-1-one (ODQ, the guanylate cyclase inhibitor), or $10\;{\mu}M$ indomethacin (the cyclooxygenase inhibitor). Putative $K^+$ channel blockers (charybdotoxin plus apamin or glibenclamide) did not affect the extract-induced relaxation in cerebral or coronary artery rings. In contrast, in rat aortic rings the extract produced significantly smaller relaxant response in endothelium-denuded rings than that in endothelium-intact rings. Pretreatment with L-NAME or ODQ abolished the extractinduced endothelium-dependent aortic relaxation, whilst indomethacin $(3\;{\mu}M)$ had no effect. The present results indicate that hawthorn fruit extract possesses a vasorelaxing effect in cerebral, coronary and carotid arteries and this effect is independent of the presence of a functional endothelium. However, the extract-induced endothelium-dependent relaxation in rat aorta was mediated through endothelial nitric oxide and cyclic GMP-dependent mechanisms, suggesting that active components in the extract may act on endothelium to stimulate release of nitric oxide in large conduit arteries of the rats.

• YAKHAK HOEJI
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• v.41 no.2
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• pp.241-246
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• 1997

The effect of potassium channel openers, SKP-450, SKP-818 and lemakalim have been compared in rat heart and aorta. In rat isolated heart, SKP-450 had a greater negative inotrop ic effect than lemakalim and KR-30818 against left ventricular developed pressure (LVDP) and double product of heart rate and LVDP (DP). In addition, SKP-450 had a greater effect than lemakalim and KR-30818 in increasing coronary flow, indicating a more potent vasodilating effect in coronary artery. Negative inotropic effect and coronary vasodilating effect of SKP-450 and SEP-818 were significantly reduced by 10 min-perfusion with $10^{-6}M$ glyburide, a selective blocker of ATP-sensitive potassium channel. In rat aorta, SKP-30450 and SKP-30818 as well as lemakalim induced powerful concentration-dependent relaxations against norepinephrinc-induced tone ($EC_{50},\;{\mu}M$ : SKP-30450, $0.107{\pm}0.009$; SKP-30818, $0.476{\pm}0.022$ ; lemakalim, $0.565{\pm}0.039$ ). These relaxant effects were significantly reduced by pretreatment with glyburide. In sununary, SKP-30450 and SKP-30818 showed greater negative inotropic and vasorelaxant effect than lemakalim in rat aorta with order of potency of SKP-30450 > SKP-30818 > lemakalim. These actions are suggested to be mediated at least in part by a mechanism which involves the opening of ATP-sensitive potassium channel.

• The Journal of Korean Physical Therapy
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• v.15 no.2
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• pp.146-156
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• 2003

Isolated rat thoracic aorta which is pharmacologically precontracted by phenylephrine induces photorelaxation when exposed to long wave length UV-light. The aim of the present study was to characterize the mechanism of UV-light induced by photorelaxation in the rat aorta. 1. UV light relaxed both endothelium-intact and -denuded rat aortic rings contracted by phenylephrine. The magnitude of relaxation on UV light was dependent on the exposure time and slightly greatly in endothelium-denuded rings than in endothelium-intact preparations. 2. L-NAME (10 nM - 100 $\mu$M) but not D-NAME completely inhibited the photorelaxation in a concentration dependent manner. 3. The UV-induced relaxation was inhibited by methylene blue (1 - 100 uM), and verapamil (100 nM), and removal of extracellular $Ca^{2+}$. In contrast, UV-light induced photorelaxation was potentiated by $N^{w}$-nitro-L-arginine (L-NNA) treatment. These results suggest that UV light-induced photorelaxation may be due to nitric oxide from exogenously administered L-arginine as well as endogenous nitric oxide donors such as amino acid and arginine derivatives

• Nutrition Research and Practice
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• v.3 no.2
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• pp.102-107
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• 2009

Fish oil and shortening have been suggested to have opposite effects on cardiovascular disease (CVD). This study investigated the effect of shortening and fish oil on CVD risk factors and aorta histopathology, and the association between risk factors and aorta histopathology. Male Wister rats (n=30) were fed an AIN-93G diet containing 20% fat in the form of fish oil, shortening, or soybean oil for 4 weeks. Total cholesterol (TC), triacylglyceride (TG), and C-reactive protein levels were significantly (P<0.001) lower in the fish oil than in soybean oil and shortening groups. HDL-cholesterol concentrations were significantly different (P<0.001) between groups. In addition, LDL-cholesterol levels were significantly (P<0.001) lower in the fish oil and shortening groups than in the soybean oil group. Insulin and glucose concentrations did not differ among groups. Effect of dietary fat on tissue fatty acid composition significantly differed in abdominal fat and brain compared with RBC, heart, kidney and liver. The aortic wall was significantly (P=0.02) thinner in the fish oil group than in the soybean oil and shortening groups. The aortic wall thickness was positively correlated with TG and TC, but negatively with EPA + DHA levels of all tissues. These results suggested that fish oil had protective effects on aorta histopathology by hypolipidemic action in this rat model.

• Journal of Ginseng Research
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• v.21 no.2
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• pp.125-132
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• 1997

Our previous study showed that in vivo treatment of spontaneously hypertensive rats (SHR) with protopanaxatriol ginsenosides (PPT) reduces the blood pressure and inhibits the con- tractions induced by endothelium-derived contracting factor (prostaglandin endoperoxide ($PGH_2$) and superoxide anion) in aorta isolated from SHR. The aim of the present study is to examine whether PPT improves endothelial functions in the isolated thoracic aorta of SHR in vitro. Treatments of aortic rings with PPT, purified ginsenoside $Rg_1$ ($Rg_1$) or indomethacin normalized endotheliuln-dependent relaxation to acetylcholine, but not with protopanaxadiol ginsenosides (PPD) and purified ginsenoside Rb1 (Rb1). The effects of PPT were dose-dependent. PGH,- and oxygen free radical-inducted contractions in rat aorta without endothelium were inhibited by PPT or $Rg_1$, but not by PPD or $Rb_1$. Contractions induced by PGF2$\alpha$, U-46619, a stable thromboxane A2 agonist or KCI (60 mM) were not inhibited by PPT, $Rg_1$ or $Rb_1$. These findings demonstrate that PPT but not PPD scavenges the oxygen-derived free radicals and/or antagonize the effects of $PGH_2$ in the vascular smooth muscle and may explain the hypotensive effect of ginseng in the SHR.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1998.11a
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• pp.146-146
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• 1998

The present study was designed to examine the effect of total ginseng saponin on contractile responses of vasoconstrictors in the rat aorta. Phenylephrine (an adrenergic ${\alpha}$$_1$-receptor agonist) and high potassium (a membrane depolarizing agent) caused greatly contractile responses in the rat aorta, respectively. However, in the presence of total ginseng saponin (600 $\mu\textrm{g}$/$m\ell$), the contractile responses of phenylephrine (10$\^$-5/ and 10$\^$-7/ M) and high potassium (3.5 ${\times}$ 10$\^$-2/ and 5.6 ${\times}$ 10$\^$-2/ M) were markedly potentiated whereas prostaglandin F$\sub$2${\alpha}$/ (5 ${\times}$ 10$\^$-6/ M)-induced contractile response was not affected. The contractile responses induced by phenylephrine (10$\^$-5/ M) and high potassium (3.5 ${\times}$ 10$\^$-2/ M) even in the presence of total ginseng saponin (600 $\mu\textrm{g}$/$m\ell$) were greatly inhibited by the pretreatment of nicardipine (10$\^$-6/ M), a calcium channel blocker. Taken together, these experimental results suggest that total ginseng saponin can enhance the contractile responses evoked by stimulation of adrenergic ${\alpha}$$_1$-receptor and the membrane depolarization in the rat aorta, which seems to be associated to calcium influx.

• The Korean Journal of Zoology
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• v.16 no.3
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• pp.177-184
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• 1973

The effect of heat treatment (autoclaving at $100^{\circ}C$ for 30 minutes) of soybean on the cholesterol contents in the brain and aorta of the albino rat was studied. The subjects were 72 young male rats and divided into 12 groups by diet and periods. Experimented periods were 5, 15 and 30 days, diet standard are raw soybean, soybean diets heated at $100^{\circ}C$ and $120^{\circ}C$ respectively, and each diet was prepared to contain 14g protein and 400 Kcal per diet 100g. After corresponding treatment, the cholesterols in the brain and aorta were determined. The results are summarized as follows: In the brain, total, free and ester cholesterol contents of each group are not remarkedly different from those of control group, in the experimental periods. In the aorta total and free cholesterol at $100^{\circ}C$ and $120^{\circ}C$ than those of control group, but there is no significant difference among groups fed for 15 or 30 days, and the ester cholesterol has no regular tendency. It seems that the heat treatment at $100^{\circ}C$ and $120^{\circ}C$ of solybean has no effect on the cholesterol contents of the brain and aorta.

• Journal of Life Science
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• v.13 no.5
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• pp.634-641
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• 2003

In order to examine whether arsenic, one of environmental stress, contribute to augumentation and relaxation of rat aorta, this study was performed in vivo and in vitro, using intacted or denuded rats aorta ring preparation, respectively. The carotid arterial pressure was recorded on an ink-writing physiograph(Grass Co. 79E) connected to strain gauge. The contractile response of vascular ring with or without endothelium preparation isolated from rat were determined in organ bath and was recorded on physiograph connected to isometric transducer. Vasopressin-,and phenylephrine- induced increase in arterial pressure significantly enhanced in arsenic-treated rats; increase of 19.1%, and 46.6%, respectively. Vascular contractile response was measured in vitro preparations exposed to 0, 0.5, 1, 2 and 4 mM of arsenic for 1, 3, 5 and 8 hours. The dose-vascular responses of phenylephrine augmented by increasing dose of arsenic in the strips exposed to arsenic for 8 hours, and did not augmented for 1, 3, 5 hours. The phenomenon was not affected by strips denuded endothelium. And the response of relaxation of rat aorta induced by nitroprusside was not influenced by arsenic stress, but acetylcholine was a little increased. compared to that of control. There were no significant difference in relaxation between control and arsenic treated rings with endothelium or denuded. All of the results, phenyleprine-induced vascular contraction was significantly enhanced in 4 mM arsenic-treated rat aortic rings compared with control, whether endothelium was present or denuded at 8 hours after arsenic treatment. It may be a mechanism by which long-term arsenic stresses play a role in development of hypertension.

• Journal of Life Science
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• v.10 no.6
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• pp.584-590
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• 2000

Natural products are one of the useful source of cardiovascular drugs, in particular, when they have antioxidant activity. Gagaminine, an alkaloid isolated from the roots of Cynanchum wilfordi Hemsley, has been reported to potently inhibit the aldehyde oxidase activity ({TEX}$IC_{50}${/TEX}=0.8$\mu$M) and reduce lipid peroxidation. However, the effect of gagaminine on vascular smooth muscle has not yet been investigated. In the present study, we examined whether gagaminine relaxes vascular smooth muscle by isometric tension study. In order to observe its relaxation effect on the arteries, conductivel vessel (rat thoracic aorta) and resistance vessel (pig coronary artery) were purposely used. Results indicated that gagaminine relaxed in a concentration-dependent manner $\alpha$-adrenoceptor agonist, phenylephrine (PE)-induced contraction of rat aorta. Pretreatment with gagaminine inhibited PE-induced contraction, noncompetitively. {TEX}$Ca^{2+}${/TEX}-induced contraction was significantly diminished by gagaminine. In pig coronary artery, gagaminine relaxed thromboxane receptor (U 46619)-mediated contraction in dose-dependent manner. Pretreatment with gagaminine also reduced the maximum contraction induced by KCl. These observations strongly suggest that agagminnine relaxes vascular smooth muscle, irrespective of both resistance and conductive artery. We demonstrate that gagaminine, a potent natural antioxidant, has a significant vasodilatory effect and its action mechanism van be ascribed at least in part to {TEX}$Ca^{2+}${/TEX} antagonistic action as evidenced by inhibition {TEX}$Ca^{2+}${/TEX}-induced contraction (rat aorta) and KCl-induced contraction (porcine artery). Furthermore, neither $\alpha$ -adrenoceptor nor thromboxane receptor seems responsible for the relaxation of gagaminine.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.4
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• pp.471-477
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• 1998

Cyclosporin A (CsA), a widely used immunosuppressant, is well known to cause nephrotoxicity and hypertension as major side effects. The present study was aimed at investigating the effects of CsA-pretreatment on the activities of cytosolic guanylate cyclase (cGC) in relation to the alteration of relaxant responses in the rat thoracic aorta. CsA $(10\;{\mu}M)-preincubation$ for 90 min significantly attenuated the vasodilatation induced by sodium nitroprusside (SNP), a cytosolic guanylate cyclase activator, shifting the dose-response curve to the right. The increase in cGMP contents induced by SNP was markedly attenuated by CsA. SNP ($1\;{\mu}M{\sim}\;mM$) increased the cGC activity dose-dependently, and the increase was completely abolished by CsA. CsA attenuated the SNP-induced cGC activation dose-dependently. The abolishing effect of CsA-pretreatment on the SNP-induced cGC activation was not affected by washing the preparation, suggesting that the inhibition is irreversible. When CsA was added simultaneously with SNP, cGC activation was not attenuated. 1-(5-isoquinolinylsulfonyl)-2-methyl piperazine (H-7), a protein kinase C (PKC) inhibitor, decreased SNP-induced cGC activation and blocked the CsA-attenuation of cGC activation. These results suggest that CsA directly inhibits cGC participating in the CsA-induced impairment of vasodilatation, and that PKC is involved in the inhibitory action of CsA on cGC.