• Biomolecules & Therapeutics
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• v.24 no.1
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• pp.57-61
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• 2016

Fisetin, a natural flavonoid found in a variety of vegetables and fruits, has been shown to possess many biological functions. The present study was undertaken to investigate the influence of fisetin on vascular smooth muscle contractility and to determine the mechanism involved. Denuded aortic rings from male rats were used and isometric contractions were recorded and combined with molecular experiments. Fisetin significantly relaxed fluoride-, thromboxane $A_2$- or phorbol ester-induced vascular contraction suggesting as a possible anti-hypertensive on the agonist-induced vascular contraction regardless of endothelial nitric oxide synthesis. Furthermore, fisetin significantly inhibited fluoride-induced increases in pMYPT1 levels and phorbol ester-induced increases in pERK1/2 levels suggesting the mechanism involving the inhibition of Rho-kinase activity and the subsequent phosphorylation of MYPT1 and MEK activity and the subsequent phosphorylation of ERK1/2. This study provides evidence regarding the mechanism underlying the relaxation effect of fisetin on agonist-induced vascular contraction regardless of endothelial function.

• The Korea Journal of Herbology
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• v.26 no.1
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• pp.75-80
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• 2011

Objectives : The aim of the present study is to investigate the hypotensive effect of Samhwangsasim-tang (SHSST), Samigangap-tang (SMGAT) and Bangtan-tang (BTT) in stroke-prone spontaneously hypertensive rats (SHR-SP). Methods : SHR-SP rats were treated with SHSST, SMGAT and BTT at dose of 200 mg/kg/day orally for 5 weeks, respectively. Results : Treatment SHR-SP rats with SMGAT significantly lowered blood pressure but not in the SHSST or BTT treat groups. On the other hand, SHSST, SMGAT and BTT ameliorated endothelium-dependent and independent vascular relaxation in the phenylephrine-precontracted aorta and carotid artery, respectively. Conclusions : These results indicated that SMGAT has an antihypertensive effect and SHSST, SMGAT and BTT improve vascular function in stroke-prone hypertensive rat model, respectively.

• Korean Journal of Veterinary Research
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• v.43 no.3
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• pp.361-371
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• 2003

The vasorelaxant actions and blood pressure lowering of the ${\alpha}_2$-adrenoceptor agonists (${\alpha}_2$-AAs) clonidine and xylazine were investigated in rat isolated aortic rings and anesthesized rats. Both clonidine and xylazine produced a concentration-dependent inhibition of the sustained contraction induced by norepinephrine (NE), but not by KCl. NE-induced contractions were attenuated partly by nifedipine or verapamil, voltage dependent $Ca^{2+}$ channel blockers. These $Ca^{2+}$ channel blockers-resistant contractions were abolished by clonidine or xylazine. Inhibitory effects of a ${\alpha}_2$-AAs on contractions could be reversed by ryanodine, an intracellular $Ca^{2+}$, transport blocker, and tetrabutylammonium (TBA), a $Ca^{2+}$ activated $K^+$ channel blocker, but not by nifedipine, glibenclamide or removal of extracellular $Ca^{2+}$ and endothelium. Moreover, ${\alpha}_2$-AAs produced relaxation in NE-precontracted isolated intact aortic rings in a concentration-dependent manner, but not in KCl-precontracted rings. The relaxant effects of ${\alpha}_2$-AAs were inhibited by ryanodine and TBA, but not by nifedipine, glibenclamide, N (G)-nitro-L-arginine (L-NNA), N(omega)-nitro-L-arginine methyl ester (L-NAME), aminoguanidine (AG), 2-nitro-4-carboxyphenyl N,N-diphenylcarhurnte (NCDC), lithium sulfate, staurosporine or removal of extracellular $Ca^{2+}$ and endothelium. In vivo, infusion of xylazine elicited significant decrease in anerial blood pressure. This xylazinelowered blood pressure was completely inhibited by the intravenous injection of TBA, but not by the intravenous injection of glibenclamide, L-NNA, L-NAME, AG, nifedipine, lithium sulfate or saponin.. These findings showed that the receptor-mediated and ${\alpha}_2$-adrenoceptor A-stimulated endothelium-independent vasorelaxant effect may be explained by decreasing intracellular $Ca^{2+}$ release and activation of $Ca^{2+}$-activated $K^+$ channels, which may contribute to the hypotensive effects of ${\alpha}_2$-AAs in rats.

• Herbal Formula Science
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• v.28 no.3
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• pp.271-280
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• 2020

Hypertension has been approved to cause disharmony between the heart and kidney such as cardiac hypertrophy and kidney dysfunction. In traditional oriental medicine Paeo-tang (PET) has been shown to have effects on blood circulation improvement. However, the beneficial effect of PET on hypertension remains unknown. In this study, we investigated that PET attenuates blood pressure and improves cardiovascular and renal function in NG-nitro-L-arginine methylester (L-NAME) rat model. Hypertensive rat models were induced by the administration of L-NAME (40 mg/kg/day) and then PET (50 or 100 mg/kg/day) or Olmetec was treated for 2 weeks. PET treatment significantly suppressed the systolic blood pressure and decreased intima-media thickness in the thoracic aorta. PET ameliorated endothelium-dependent and independent vascular relaxation in the L-NAME-induced vascular dysfunction. PET ameliorated the functional decline in the kidney such as albumin and blood urea nitrogen in plasma. These results demonstrated that PET possesses protective effects against L-NAME-induced hypertension.

• Journal of Physiology & Pathology in Korean Medicine
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• v.30 no.2
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• pp.95-100
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• 2016

The aim of the present study is to investigate the hypotensive effect of Mantidis ootheca (WMO), Rosa laevigata (WIC), and Imperata cylindrica (WRL) in renovascular hypertension rats. Experimental hypertension model is 2-kidney and 1-clip (2K1C) induced rats. 2K1C rats were treated with WMO, WIC, and WRL at dose of 100 mg/kg/day orally for 3 weeks, respectively. Treatment groups with WMO, WIC, and WRL significantly lowered blood pressure. Interestingly, WMO, WIC, and WRL ameliorated endothelium-dependent and independent vascular relaxation in the phenylephrine-precontracted thoracic aorta in hypertension models. In addition, 2K1C-induced hypertension model increased plasma renin activity, however, WMO, WIC, and WRL attenuated those activities. These results suggest that WMO, WIC, and WRL ameliorates vascular dysfunction in 2K1C-induced hypertension models via the regulation of nitric oxide and renin-angiotensin-aldosterone system.