Objectives : This study was undertaken to define the effect of Diospyros kaki L. Radix or Diospyros kaki L. Folium on phenylephrine-induced arterial contraction and the mechanism of Diospyros kaki L. Radix or Diospyros kaki L. Foliuminduced relaxation. Methods : In order to investigate the effect of Diospyros kaki L. Radix or Diospyros kaki L. Folium on contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. Diospyros kaki L. Radix or Diospyros kaki L. Folium extract was infused into contracted arterial strips induced by phenylephrine. To analyze the mechanism of Diospyros kaki L. Radix or Diospyros kaki L. Folium-induced relaxation, Diospyros kaki L. Radix or Diospyros kaki L. Folium extract was infused into contracted arterial strips induced by phenylephrine after treatment with indomethacin, $N{\omega}-nitro-L-arginine$, methylene blue or tetraethylammonium chloride, and $Ca^{2+}$ was infused into contracted arterial strips induced by phenylephrine after treatment of Diospyros kaki L. Radix or Diospyros kaki L. Folium in a $Ca^{2+}$-free solution. Results : Diospyros kaki L. Radix or Diospyros kaki L. Folium showed relaxation effect on arterial strip with endothelium contracted by phenylephrine, but in the strips without endothelium, Diospyros kaki L. Radix or Diospyros kaki L. Folium-induced relaxation was significantly inhibited. The endothelium-dependent relaxation induced by Diospyros kaki L. Radix or Diospyros kaki L. Folium was decreased by pretreatment with $N{\omega}-nitro-L-arginine$ or methylene blue but it was not observed in the strips pretreated with indomethacin or tetraethylammonium chloride. When $Ca^{2+}$ was applied to the strips which were contracted by phenylephrine in a $Ca^{2+}$-free solution, arterial contraction was increased. However, pretreatment with Diospyros kaki L. Radix or Diospyros kaki L. Folium inhibited contractile response to $Ca^{2+}$. Conclusions : Diospyros kaki L. Radix or Diospyros kaki L. Folium may suppress influx of extra- cellular $Ca^{2+}$ through the formation of nitric oxide in the vascular endothelial cells.
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
The present study was aimed at investigating possible transmitter mechanisms in the endothelial cell layer in regulating the tone of the vascular smooth muscle. The thoracic aorta was isolated from the anesthetized male white rabbits and its helical strips were prepared. Electrical field stimulation was delivered to platinum wire electrodes positioned parallel to the vessel segment preconstricted with phenylephrine [3.5x10-6 mol/L at a distance of 1.5-2.0 mm. The electrical stimulation [70 V, 5 msec, 0.5-200 Hz caused either relaxation only [34% or a biphasic response [prolonged relaxation following a weak and transient contraction, 66% . The relaxation response was frequency- dependent, and at 200 Hz a complete relaxation was noted. Mechanical rubbing of the endothelial layer abolished or greatly attenuated the relaxation. The relaxation was also markedly attenuated in the presence of NG-nitro- L-arginine methyl ester [10-3mol/L or procaine hydrochloride [3.5x10-4mol/L . Tetrodotoxin,guanethidine, atropine or indomethacin failed to block or enhance the relaxation response to electrical field stimulation. It is concluded that the vascular endothelium in the aorta contains diffusible substances that regulates the function of the smooth muscle layer, in which relaxation is more prominent than contraction. Their release by the electrical stimualtion in vitro may not involve classic neuronal transmitter release mechanisms or metabolism of arachidonic acids by cyclooxygenase. The release of the relaxing agents may require an increase in cytosolic calcium level. The chemical nature of the relaxant may be, to a large extent, nitric oxide.
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 NG-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.
We studied the effects of trazodone on arterial blood pressure in anesthesized guinea pigs, and on vascular responses in isolated thoracic aorta. Trazodone produced a concentration-dependent relaxation in phenylephrine-precontracted endothelium intact (+E) rings, but not in a KCl-precontracted aortic rings. These relaxant effects of trazodone on +E rings were significantly greater than those on denuded (-E) rings. The trazodone-induced relaxation was suppressed by glibenclamide and tetrabutylammonium, but not by N(G)-nitro-L-arginine (L-NNA), N(omega)-nitro-L-arginine methyl ester (L-NAME), methylene blue (MB), nifedipine, indomethacin, 2-nitro-4-carboxyphenyl-n,n-diphenylcarbamate (NCDC) and clotrimazole. In vivo, infusion of trazodone elicited a significant decrease in arterial blood pressure. Trazodone-induced blood pressure lowering was markedly inhibited by intravenous pretreatment of prazosin but not by pretreatment of saponin, L-NNA, L-NAME, MB, nifedipine, glibenclamide, clotrimazole and NCDC. In addition, trazodone produced an increase in twitch force of isolated papillary muscle and left ventricular pressure of perfused heart. These findings suggest that the endothelium-independent vasorelaxant effect of trazodone may be explained by activation of $Ca^{2+}$-activated and ATP-sensitive $K^+$ channels, and the hypotensive effect of trazodone is not associated with cardiac contraction.
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.
This study was investigated to evaluate the vasorelaxant effect of Rubus coreanus(RC) extract on contracted rabbit carotid artery and its mechanism. To study the effect of RC extract on contracted rabbit carotid arterial strips, arterial strips with intact or damaged endothelium were used for experiment using organ bath. The pre-contracted arterial strips with norepinephrine(NE) or potassium chloride(KCl) was treated with various concentrations of an extract of RC(0.01, 0.03, 0.1, 0.3 and 1.0 $mg/m{\ell}$). To determine the mechanisms of RC-induced vasorelaxant, RC extract was infused into contracted arterial rings which had been pretreated by indomethacin(IM), tetraethylammonium chloride(TEA), $N{\omega}$-nitro-L-arginine (L-NNA), methylene blue(MB). And calcium chloride(Ca) 1 mM was infused into precontracted arterial ring induced by NE or KCl after treatment of RC extract in $Ca^{2+}$-free krebs solution. Cytotoxic activity of RC extract on human umbilical vein endothelial cell(HUVEC) was measured by MTT assay, and nitric oxide(NO) prodution was measured by Griess reagent. RC extract revealed significant relaxation on NE-induced arterial contraction, but didn't relax on KCl-induced arterial contraction. RC extract also had an effective relaxation to the intact endothelium arterial ring, but not the damaged endothelium arterial ring. Treatment of IM, TEA, L-NNA, MB reduced the relaxation of RC extract. Pretreatment of RC extract inhibited the contraction by influx of extracellular $Ca^{2+}$ in contracted arterial ring induced by NE, but it didn't work the contraction by influx of extracellular $Ca^{2+}$ in contracted arterial ring induced by KCl in $Ca^{2+}$-free krebs solution. RC extract increased nitric oxide production on HUVEC. This study indicated that the relaxation effect of RC extract on contracted rabbit carotid artery is related with NO-cGMP pathway, EDHF, prostacyclin.
This study was undertaken to define the effect of SoPung-Tang extract on hypertension in spontaneous hypertensive rat and norepinephrine- induced arterial contraction in rabbit. In order to investigate the effect of SoPung-Tang extract on contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. To analyze the mechanism of SoPung-Tang extract-induced relaxation, SoPung-Tang extract infused into contracted arterial strips induced by norepinephrine after treatment of indomethacin, Nu-nitro-L-arginine, methylene blue or tetraethylammonium chloride. Blood pressure was significantly decreased five days after administration of SoPung-Tang extract. SoPung-Tang extract relax arterial strip with endothelium contracted by norepinephrine, but in the strips without endothelium, SoPung-Tang extract- induced relaxation was significantly inhibited. SoPung-Tang relax arterial strip contracted by norepinephrine, but in the strips contracted by high $K^+$, SoPung-Tang extract-induced relaxation was significantly inhibited. The endothelium-dependent relaxation induced by SoPung-Tang extract was decreased by the pre-treatment of $N{\omega}$-nitro-L-arginine or methylene blue, but it was not observed in the strips pre-treated with indomethacin or tetraethylammonium chloride. When $Ca^{2+}$ was applied, the strips which were contracted by norepinephrine in a $Ca^{2+}$-free solution, arterial contraction was increased. But pre-treatment of SoPung-Tang extract inhibited contractile response to $Ca^{2+}$. We suggest that SoPung-Tang could be applied effectively for hypertension and may suppress influx of extra-cellular $Ca^{2+}$ through the formation of nitric oxide in the vascular endothelial cells.
Lee, Ho Sung;Lee, Young Joo;Chung, Yoon Hee;Lee, Moo Yeol;Kim, Sung Tae;Ko, Sung Kwon;Momoi, Mariko;Kondoh, Yutaka;Sasaki, Fumio;Jeong, Ji Hoon
Journal of Ginseng Research
/
제40권4호
/
pp.334-343
/
2016
Background: Progressed tissue culture techniques have allowed us to easily obtain mass products of tissue-cultured mountain ginseng over 100 yr old (TCMG-100). We investigated the effects of TCMG-100 extract on erectile function using in vitro and in vivo studies. Methods: To examine the relaxation effects and mechanisms of action of TCMG-100 on rabbit cavernosal strips evaluated in an organ bath. To investigate the long-term treatment effect of TCMG-100, 8-wk administration was performed. After administration of TCMG-100, intracavernosal pressure, cyclic guanosine monophosphate and nitric oxide (NO) levels of cavernosal tissue, serum testosterone level, histological observation of collagen fiber, endothelium, smooth muscle cell, and transforming growth factor-${\beta}1$ were investigated. Results: TCMG-100 extract displayed dose-dependent relaxation effects on precontracted rabbit corporal smooth muscle. The TCMG-100-induced relaxation was significantly reduced by removing the endothelium, and treatment with an NO synthase inhibitor or NO scavenger. Eight weeks of TCMG-100 administration increased intracavernosal pressure in a rat model. The levels of cyclic guanosine monophosphate and NO in the corpus callosum and serum testosterone level were also increased by TCMG-100 treatment. Furthermore, histological evaluation of collagen, smooth muscle, and endothelium showed increases in endothelium and smooth muscle, and a decrease in transforming growth factor-${\beta}1$ expression. Conclusion: These relaxation effects on corporal smooth muscle and increased erectile function suggest that TCMG-100 might be used as an alternative herbal medicine to improve erectile function.
Objectives : This experiments were performed to determine the effect of OYakSoonGi-San extract on hypertension in spontaneous hypertensive rat and norepinephrine-induced arterial contraction in rabbit. Methods : In order to define the effect of OYakSoonGi-San extract on contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. To analyze the mechanism of OYakSoonGi-San extract-induced relaxation, OYakSoonGi-San extract infused into contracted arterial strips induced by norepinephrine after treatment of indomethacin, $N{\omega}-nitro-L-arginine$, methylene blue or tetraethylammonium chloride. Results : Blood pressure was significantly decreased five days after administration of OYakSoonGi-San extract. The relaxation effect of OYakSoonGi-San extract was dependent on the presence of endothelium, showing that OYakSoonGi-San extract-induced relaxation was not observed in the strips without endothelium. Also OYakSoonGi-San extract-induced relaxation was significantly inhibited in arterial strips which were contracted by high $K^+$. OYakSoonGi-San extract-indeced relaxation was significantly inhibited by the pre-treatment of $N{\omega}-nitro-L-arginine$ or methylene blue, but it was not observed in the strips pre-treated with indomethacin or tetraethylammonium chloride. When additive application of $Ca^{2+}$ in arterial strips which were pre-contracted by norepinephrine in a $Ca^{2+}$-free solution, arterial contraction was increased. But contractile response to $Ca^{2+}$ was attenuated by pre-treatment of OYakSoonGi-San extract. Conclusions : These results demonstrated that OYakSoonGi-San could be applied effectively to hypertension and may inhibit agonist-induced contraction through an decrease influx of extra-cellular $Ca^{2+}$ by the formation of nitric oxide in the vascular endothelial cells.
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