• 혜화의학회지
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• 제21권2호
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• pp.85-94
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• 2013

단삼(丹蔘) (Salvia miltiorrhiza)은 꿀풀과(일과(―科) Lamiaceae)에 속하는 다년생 초본으로, 중국이 원산지이며 약용하기 위해 우리나라에서도 널리 재배하고 있다. 신농본초경(神農本草經) 상품(上品)에 수재(收載)되어 있으며, 거어지통(祛瘀止痛), 양혈소종(凉血消腫), 청심제번(淸心除煩), 활혈조혈(活血調血) 등의 효능이 있어 부인과 질환에 많이 사용되고 있는 약재에 속한다. 본 연구에서는 단삼(丹蔘) 추출물이 흰쥐의 흉부 대동맥 절편에 어떠한 양상으로 작용하는지 확인하고자 하였으며, 그 결과 단삼 추출물 특히 헥산 분획에서 강력한 혈관 이완 작용이 나타났으며, 혈관 내피 세포의 존재 유무에 상관없이 농도 의존적으로 혈관을 이완시켰으나 혈관 내피 세포가 존재하는 상황에서 더욱 강력한 혈관 이완 작용을 보였다. 이러한 과정에 NO에 의한 cGMP 증가가 주요하게 작용하는 것으로 추정되었으며, 칼슘 통로 차단 효과에 의한 세포 내 $Ca^{2+}$의 감소도 관여하는 것으로 생각된다.

• Journal of Ginseng Research
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• 제21권1호
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• pp.49-52
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• 1997

There are many mechanisms that mediate progression of renal injury, such as abnormalities of nitric oxide (NO) regulation, increased Platelet aggregatlon, and oxygen free radical injury. Ginseng has been known to have NO dependent vasorelaxant effect and antioxidant effect, also inhibit thrombin stimulated platelet aggregation. And these effects of ginseng may have some roles in prevention of renal injury. So we studied 24 patients with mild pathologic proteinuria and hypertension to evaluate the effect of ginseng on progression of renal injury. After 1 month treatment, creatinine clearance was significantly increased especially in the patient group with normal serum creatinine level without specific side effect. The result of this study suggest that ginseng may pre vent or retard the progression of renal injury especially in early stage.

• Toxicological Research
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• 제28권4호
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• pp.249-253
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• 2012

In this study, we prepared alcohol extracts of the larva, pupa, queen, and cocoon (clony) of B. ignitus, B. terrestris, and B. h. sapporoensis, and tested the anti-inflammatory activity of the extracts by using a rat model of adjuvant-induced edema. The extracts derived from the queen of B. ignitus, the queen of B. terrestris, and the cocoon of B. ignitus decreased hind paw edema after 1 day of i.p. administration. These extracts also induced vasorelaxation and NO production in calf pulmonary artery endothelial cells. These results suggest that bumblebee alcohol extracts has anti-inflammatory and vasorelaxant properties.

• 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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• 제33권4호
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• pp.198-206
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• 2019

This study was conducted to evaluate the vasorelaxant effect of DangGuiSu-San and SamHwangSaSim-Tang extract on contracted rabbit carotid artery. To study the effect of DangGuiSu-San and SamHwangSaSim-Tang 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 Phenylephrine(PE) was treated with various concentrations of DangGuiSu-San and SamHwangSaSim-Tang extract(0.01, 0.03, 0.1, 0.3 and $1.0mg/m{\ell}$). To determine the mechanisms of DangGuiSu-San and SamHwangSaSim-Tang-induced vasorelaxant, DangGuiSu-San and SamHwangSaSim-Tang extract were 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 PE after treatment of DangGuiSu-San and SamHwangSaSim-Tang extract in $Ca^{2+}$-free krebs solution. DangGuiSu-San and SamHwangSaSim-Tang extract revealed significant relaxation on PE-induced arterial contraction. DangGuiSu-San and SamHwangSaSim-Tang extract also had an effective relaxation to the intact endothelium arterial ring. SamHwangSaSim-Tang extract on contracted rabbit carotid artery is related with NO-cGMP pathway. Pretreatment of DangGuiSu-San and SamHwangSaSim-Tang extract inhibited the contraction by influx of extracellular $Ca^{2+}$ in contracted arterial ring induced by NE. This study indicated that the relaxation effect of SamHwangSaSim-Tang extract on contracted rabbit carotid artery is related with NO-cGMP pathway. Pretreatment of DangGuiSu-San and SamHwangSaSim-Tang extract inhibited the contraction by influx of extracellular $Ca^{2+}$ in contracted arterial ring induced by NE.

• The Korean Journal of Physiology and Pharmacology
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• 제4권6호
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• pp.463-469
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• 2000

It has been well known that 4-aminopyridine (4-AP) has an excitatory effect on vascular smooth muscle due to causing membrane depolarization by blocking $K^+-channel$. However, we observed that 4-AP had an inhibitory effect on the mesenteric artery of rat. Therefore, we investigated the mechanism of 4-AP-induced vasorelaxation. The mesenteric arcuate artery and its branches were isolated and cut into ring. The ring segment was immersed in HEPES-buffered solution and its isometric tension was measured. 4-AP $(0.1{\sim}10\;mM)$ induced a concentration-dependent relaxation, which was unaffected by NO synthase inhibitor, $N^G-nitro-L-arginine$ methylester $(100\;{\mu}M)$ or soluble guanylate cyclase inhibitor, methylene blue $(100\;{\mu}M).$ Glibenclamide $(100\;{\mu}M)$, ATP-sensitive $K^+$ channel blocker, did not exert any effect on the 4-AP-induced vasorelaxation. 4-AP relaxed the sustained contraction induced by 100 mM $K^+$ or $Ca^{2+}$ ionophore, A23187 $(100\;{\mu}M)$ in a dose-dependent manner. In addition, 4-AP significantly decreased the phasic contractile response to norepinephrine in the absence of extracellular $Ca^{2+}$. However, 4-AP did not block the $^{45}Ca$ influx of rat aorta. From the above results, we suggest that 4-AP may not block the $Ca^{2+}$ influx through $Ca^{2+}-channel,$ but act as a nonspecific vasorelaxant in arterial smooth muscle.

• 동의생리병리학회지
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• 제19권3호
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• pp.797-801
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• 2005

While conducting an in vitro screening of various medicinal plant extracts, an aqueous extract of Rosa rugosa Radix (ARR) was found to exhibit a distinct vasorelaxant activity. ARR induced a concentration-dependent relaxation of the phenylephrine-precontracted aorta. This effect disappeared with the removal of functional endothelium. Pretreatment of the aortic tissues with NG-nitro-L-arginine methyl ester (L-NAME) or 1H-[1,2,4]-oxadiazole-[4,3-]-quinoxalin-1-one (ODQ) completely inhibited the relaxation induced by ARR. ARR-induced vascular relaxations were also markedly attenuated by addition of diltiazem or verapamil. However, the relaxant effect of ARR was not blocked by pretreatment with indomethacine, tetraethylammonium (TEA), glibenclamide, atropine, or propranolol. Taken together, the present study suggests that ARR dilates vascular smooth muscle via endothelium-dependent NO/cGMP signaling.

• Journal of Ginseng Research
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• 제44권4호
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• pp.538-543
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• 2020

Cardiovascular diseases are a rapidly growing epidemic with high morbidity and mortality. There is an urgent need to develop nutraceutical-based therapy with minimum side effects to reduce cardiovascular risk. Panax ginseng occupies a prominent status in herbal medicine for its various therapeutic effects against inflammation, allergy, diabetes, cardiovascular diseases, and even cancer, with positive, beneficial, and restorative effects. The active components found in most P. ginseng varieties are known to include ginsenosides, polysaccharides, peptides, alkaloids, polyacetylene, and phenolic compounds, which are considered to be the main pharmacologically active constituents in ginseng. P. ginseng is an adaptogen. That is, it supports living organisms to maintain optimal homeostasis by exerting effects that counteract physiological changes caused by physical, chemical, or biological stressors. P. ginseng possesses immunomodulatory (including both immunostimulatory and immunosuppressive), neuromodulatory, and cardioprotective effects; suppresses anxiety; and balances vascular tone. P. ginseng has an antihypertensive effect that has been explained by its vasorelaxant action, and paradoxically, it is also known to increase blood pressure by vasoconstriction and help maintain cardiovascular health. Here, we discuss the potential adaptogenic effects of P. ginseng on the cardiovascular system and outline a future research perspective in this area.

• Biomolecules & Therapeutics
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• 제15권1호
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• pp.40-45
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• 2007

The vascular relaxant effects on isolated rat aorta of amlodipine camsylates (S-, R-enantiomer, and R/S-racemate), were evaluated and compared with that of S-amlodipine besylate. Furthermore, antihypertensive effects were measured in spontaneously hypertensive rat (SHR). The S-amlodipine camsylate concentration-dependently inhibited $Ca^{2+}$-induced contraction of rat aorta with a very slow onset of action (reached its maximum at 3.5h; $ED_{50}:\;1.50\;{\pm}\;0.24$ nM), having a potency 2-fold higher than those of R/S-amlodipine camsylate $(ED_{50}:\;3.36\;{\pm}\;0.91\;nM)$ and similar to those of S-amlodipine besylate $(ED_{50}:\;1.44\;{\pm}\;0.14\;nM)$, whereas the R-amlodipine camsylate has 590-fold lower vasorelaxant activity $(ED_{50}:\;886.4\;{\pm}\;49.7\;nM)$. In SHR, orally administered S-amlodipine camsylate produced a dose-dependent and long-lasting (>>10 h) antihypertensive effect $(ED_{20}:\;0.89\;mg/kg)$, with a potency 2-fold higher than those of R/S-amlodipine camsylate $(ED_{20}:\;1.82\;mg/kg)$ and similar to those of S-amlodipine besylate $(ED_{20}:\;0.71\;mg/kg)$. In contrast, the R-amlodipine camsylate has no effect even-though administrated high concentration 10 mg/kg. These results suggest that S-amlodipine camsylate has the potency and long-lasting antihypertensive activity as single enantiomer drug, and its antihypertensive effect is not significantly different to that of S-amlodipine besylate.

• 대한수의학회지
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• 제43권4호
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• pp.597-606
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• 2003

Although the antidepressant effects of imipramine (IMI) have been well known in several studies, the effects on cardiovascular system, particularly the vasorelaxant effects, have not known clearly. We hypothesis that IMI-induced vasorelaxation involves NO (nitrie oxide), activation of guanylate cyclase (GC) and $Ca^{2+}$ channel. The possible roles of the endothelium and $Ca^{2+}$ in IMI-induced responses were investigated using isolated rings of rat thoracic aorta and anesthesized rats. In KCl-precontracted rings. IMI produces endothelium-dependent and endothelium-independent relaxations in intact (+E) as well as endothelium-denuded (-E) rat aorta in a concentration-dependent manner. In phenylephrine (PE)-precontracted rings, the IMI-induced relaxation was significantly greater in +E rings. The IMI-induced relaxations were suppressed by nitric oxide synthase (NOS) inhibitors, N(G)-nitro-L-arginine (L-NNA), N(omega)-nitro-L-arginine methyl ester (L-NAME) and aminoguanidine, a non-selective GC inhibitor, methylene blue, $Na^+$ channel blockers, lidocaine and procaine, or $Ca^{2+}$ channel blockers, nifedipine and verapamil, in PE-precontracted +E rings, but not in PE-precontracted -E rings. These relaxations were also suppressed by lidocaine or procaine in -E aortic rings. However, IMI-induced relaxations were not inhibited by a PLC inhibitor 2-nitro-4-carboxyphenyl-n,n-diphenylcarbamate (NCDC), an inositol monophosphatase inhibitor, lithium, indomethacin and dexamethasone in +E and -E rings. In vivo, infusion of IMI elicited significant decrease in arterial blood pressure. After intravenous injection of saponin, NOS inhibitors. MB and nifedipine, infusion of IMI inhibited the IMI-lowered blood pressure markedly. These findings suggest that the endothelium-dependent relaxation induced by IMI is mediated by activation of NO/cGMP signaling cascade or inhibition of $Ca^{2+}$ entry through voltage-gated channel, and this mechanism may contribute to the hypotensive effects of IMI in rats.