• Korean Journal of Plant Resources
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• v.35 no.6
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• pp.713-719
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• 2022

Platycodon grandiflorum and Glycyrrhiza uralensis contain several bioactive compounds, such as saponin, oleanolic acid, and flavone. P. grandiflorum and G. uralensis have traditionally been used to treat disorders related to blood pressure, diabetes, and counteracting poison, and they have antinociceptive and antiinflammatory properties. However, the validity of complex saponin's vasodilatory effect has not been scientifically investigated. Therefore, this study explores the vasodilatory effect of complex saponin extracted from P. grandiflorum and G. uralensis mixture extract on rabbit carotid arteries. To this end, arterial rings with intact or damaged endothelium were used in an organ bath experiment and contracted by endothelin. Complex saponins, the major active constituents of P. grandiflorum and G. uralensis mixture extract, exhibited a moderate vasodilatory effect on the rabbit's basilar arteries. Therefore, treatment with complex saponin extracted from P. grandiflorum and G. uralensis mixture extract may selectively accelerate cerebral blood flow through basilar arterial dilation. Overall, the findings suggest that the extracted complex saponins can serve as vasodilator sources.

• Journal of Pharmacopuncture
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• v.19 no.4
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• pp.329-335
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• 2016

Objectives: Safranal is a pharmacologically active component of saffron and is responsible for the unique aroma of saffron. The hypotensive effect of safranal has been shown in previous studies. This study evaluates the mechanism for the vasodilatory effects induced by safranal on isolated rat aortas. Methods: To study the vasodilatory effects of safranal (0.2, 0.4 and 0.8 mM), we contracted isolated rat thoracic aorta rings by using $10^{-6}-M$ phenylephrine (PE) or 80-mM KCl. Dimethyl sulfoxide (DMSO) was used as a control. The vasodilatory effect of safranal was also evaluated both on intact and denuded endothelium aortic rings. Furthermore, to study the role of nitric oxide and prostacyclin in the relaxation induced by safranal, we incubated the aortic rings by using L-NAME ($10^{-6}M$) or indomethacin ($10^{-5}M$), each for 20 minutes. Results: Safranal induced relaxation in endothelium-intact aortic rings precontracted by using PE or KCl in a concentration-dependent manner, with a maximum relaxation of more than 100%. The relaxant activity of safranal was not eliminated by incubating the aortic rings with L-NAME ($EC_{50}=0.29$ vs. $EC_{50}=0.43$) or with indomethacin ($EC_{50}=0.29$ vs. $EC_{50}=0.35$), where $EC_{50}$ is the half maximal effective concentration. Also, the vasodilatory activity of safranal was not modified by endothelial removal. Conclusion: This study indicated that relaxant activity of safranal is mediated predominantly through an endothelium-independent mechanism.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.5
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• pp.1235-1242
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• 2003

This study was performed for the investigation of vasodilatory effects of Crataegus pinnatifida Bunge and for isolation and structure determination of the constituent from the active fraction. The fruits of this herbal drug were extracted with 80% methanol, then fractioned successively with methylene chloride, ethylacetate and n-butanol. Among the fractions, ethyl acetate fraction exhibited the most effective vascular relaxation against phenylephrine-induced arterial contraction. In order to isolate the active constituent by activity-guided fractionation, this fraction was chromatographed on silica gel to yield seven subfractions. Among the subfractions, the active one showing the most potent vascular relaxation activity was further separated by prep. HPLC with reversed phase Microsorb C-18 column using 1 % acetic acid and methanol gradient solvent system to afford one pure compound, which revealed a potent vasodilatory effect. Instrumental analyses (NMR and mass spectrometry) of the isolated constituent indicated this compound to be (-)-epicatechin. The vasodilatory action mechanism of this compound should be further investigated.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.5
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• pp.1382-1386
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• 2004

This study was performed for the investigation of vasodilatory efficacy and its underlying mechanisms of Samhwangsasim-tang(SST), herbal remedy. SST relaxed vascular strips precontracted with phenylephrine or KCI(51 mM), but the magnitude of relaxation was greater in phenylephrine(PE) induced contraction. The relaxation effects of SST was endothelium-independent. L-NAME, iNOS inhibitor, and methyl en blue(MB), cGMP inhibitor, did not attenuate the relaxation responses of SST. In the absence of extracellular Ca2+, pre-incubation of the aortic rings with SST significantly reduced the contraction by PE, suggesting that the relaxant action of the SST includes inhibition of Ca/sup 2+/ influx and release of Ca/sup 2+/ from intracellular stores (SR). In addition, the cell death was induced by SST in human aortic smooth muscle cells but not that of human umbilical vein endothelial cells. We conclude that in rat thoracic aorta, SST may induce in part vasodilation through inhibition of Ca/sup 2+/ influx and release of Ca/sup 2+/ from intracellular stores.

• Korean Journal of Veterinary Research
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• v.41 no.3
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• pp.299-304
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• 2001

The effect of the nitric oxide synthase(NOS) inhibitor, $N^{G}$-nitro-L-arginine methyl ester (L-NAME), and the prostanoid synthesis inhibitor, indomethacin, on the vasodilatation produced in response to acetylcholine(Ach) on the isolated rabbit renal artery was examined. The vasodilatory reponses to Ach($10^{-8}-3{\times}10^{-5}M$) were completely absent in thevessel which the endothelium had previous been removed. L-NAME($10^{-4}M$) significantly reduced the vasodilatory reponse to the Ach($10^{-8}-3{\times}10^{-5}M$). When L-arginine ($10^{-3}M$) was also present in the organ bath along with L-NAME($10^{-4}M$), this inhibitory effect of L-NAME ($10^{-4}M$) on the vasodilatory response to Ach ($10^{-8}-3{\times}10^{-5}M$) was significantly attenuated, Indomethacin ($10^{-6}M$) did not significantly affect the vasodilatory responses to Ach ($10^{-8}-3{\times}10^{-5}M$). The inhibition by L-NAME ($10^{-4}M$) and indomethacin ($10^{-6}M$) on vasodilatory response to Ach was significantly greater than the inhibition due to L-NAME ($10^{-4}M$) alone. The present study has established that Ach induce relaxation via and endothelium-dependent mechanism, this relaxation to Ach involves both nitric oxide(NO) and prostanoid in the isolated rabbit renal artery.

• 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.

• Korean Journal of Veterinary Research
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• v.43 no.4
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• pp.573-578
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• 2003

The effects of removing the endothelium on the vasodilatory response to substance P, calcitonin gene-related peptide (CGRP), and vasoactive intestinal peptide (VIP) was examined in the isolated rabbit renal artery. The vasodilator response to substance P ($0.1{\mu}M$) was completely absent in vessels in which the endothelium had previously been removed. There was no significant difference in the vasodilatation produced in response to CGRP ($0.1{\mu}M$), or VIP ($0.1{\mu}M$) in the intact and removed-endothelium rabbit renal artery segments. L-NAME ($100{\mu}M$) significantly reduced the vasodilatory response to substance P ($0.1{\mu}M$). This inhibition was significantly attenuated when L-arginine (10 mM) was also present in the organ bath along with L-NAME ($100{\mu}M$). Indomethacin ($1{\mu}M$) did not significantly affect the vasodilatation produced in response to substance P ($0.1{\mu}M$). The inhibitory effect of L-NAME ($100{\mu}M$) and indomethacin ($1{\mu}M$) on the vasodilatory response to substance P ($0.1{\mu}M$) was not significantly different from that produced by L-NAME ($100{\mu}M$) alone. This study indicates that substance P induced vasodilatation via an endothelium-dependent mechanism in the isolated rabbit renal artery. It also established that CGRP and VIP induced vasodilatation by an endothelium-independent mechanism and substance P-induced vasodilatation is at least partially via NO.

• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.6
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• pp.1620-1624
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• 2006

This study was performed to investigate a vasodilatory efficacy and its underlying mechanisms of the mixture of Cnidium officinale, Petasites japonicus and Coptis chinensis (CPC), CPC relaxed rat aortic vascular strips in endothelium-independant manner precontracted with phenylephrine or KCI(50mM), but the magnitude of relaxation was greater in KCI induced contraction. L-NAME, iNOS inhibitor, and methylen blue(MB), cGMP inhibitor, did not attenuate the relaxation responses of CPC. Furthermore, the contraction by increaseing $Ca^{2+}$ concentration (0.3-10.0mM) to a $Ca^{2+}$-free high $K^+$ (60mM) was significantly reduced by CPC pretreatment. These results suggest that the relaxation effect of CPC is related with the block of $Ca^{2+}$ influx via $Ca^{2+}$ channel.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.138.1-138.1
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• 2003

$\beta$-Eudesmol is one of various compounds derived from the bark of Magnolia obovata Thunberg, a medicinal plant. It has been shown that $\beta$-eudesmol also markedly alleviated muscle fasciculation, tremor and convulsion induced by diisopropylfluorophosphate and prolonged the time to death in mice (Chiou et al., 1995). Actually, the extract of magnolia bark has been shown to have depressant actions on the cental nervous system (Watanabe et al., 1973). (omitted)

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.6
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• pp.809-816
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• 1997

The present study was designed to investigate whether endogenous nitric oxide(EDNO) is involved in submandibular vasodilation and salivation induced by parasympathetic nerve stimulation. Effects of $N^w$-nitro-L-arginine-methyl ester (L-NAME) which blocks the synthesis of EDNO from L-arginine on the submandibular vasodilation and salivation induced by chords stimulation or administration of various vasodilators were examined in anesthetized cats. Effect of L-NAME on $K^+$ efflux induced by carbachol was also examined using the excised submandibular slice in vitro. In the submandibular slices, acetylcholine$(10^{-5}\;mol/L)$ or vasoactive intestinal polypeptide$(VIP,\;10^{-5}\;mol/L)$ increased $NO_2$ contents, which was Prevented by pretreatment with L-NAME. Salivary secretion in response to the chords stimulation$(3\;V,\;1\;msec,\;10{\sim}20\;Hz)$ was completely blocked by treatment with atropine(1 mg/kg). Increased blood flow response to the low frequency(1, 2, 5 Hz) stimulation was significantly reduced, whereas the blood flow induced by the higher frequency(10,20 Hz) stimulation was not affected. Lingual-arterial infusion of L-NAME(100 mg/kg) significantly diminished the vasodilatory and salivary responses to the chorda stimulation at all stimuli frequencies used. Intra-arterial infusion of L-NAME(100 mg/kg markedly diminished the vasodilatory responses to acetylcholine$(5\;{\mu}g/kg)$, VIP$(5\;{\mu}g/kg)$ or bradykinin$(5\;{\mu}g/kg)$. In the excised submandibular slice, $K^+$ efflux in response to carbachol$(10^{-5}\;mol/L)$ was significantly decrease by pretreatment with L-NAME$(10^{-5}\;mol/L)$. In the isolated submandibular artery precontracted with phenylephrine$(10^{-5}\;mol/L)$, the vasorelaxation induced by ACh$(10^{-7}\;mol/L)$ was reversed into a contraction by methylene blue$(10^{-4}\;mol/L)$. These results suggest that EDNO may play an important role in vasodilation and secretion of the submandibular gland.