Journal of Physiology & Pathology in Korean Medicine (동의생리병리학회지)

The Physiological Society of Korean Medicine and The Society of Pathology in Korean Medicine (대한동의생리학회·한의병리학회)
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Role of $K^+$ Channels in the Vasodilation of Jagumhuan

좌금환(左金丸)의 혈관이완과 $K^+$ channel

  • Son, Chang-Woo (Department of Physiology, College of Oriental Medicine, Dongguk University) ;
  • Lee, Heon-Jae (Department of Physiology, College of Oriental Medicine, Dongguk University) ;
  • Liou, Jia-Liang (Department of Physiology, College of Oriental Medicine, Dongguk University) ;
  • Shin, Heung-Mook (Department of Physiology, College of Oriental Medicine, Dongguk University)
  • 손창우 (동국대학교 한의과대학 생리학교실) ;
  • 이헌재 (동국대학교 한의과대학 생리학교실) ;
  • 유가량 (동국대학교 한의과대학 생리학교실) ;
  • 신흥묵 (동국대학교 한의과대학 생리학교실)
  • Published : 2005.06.25
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Abstract

This study was performed for the investigation of vasodilatory efficacy and its underlying mechanisms of Jagumhuan(JGH), a herbal remedy. JGH produced completely endothelium-dependent relaxation and relaxed phenylephrine(PE)-precontracted aorta in a concentration dependent manner. The magnitude of relaxation was greater in PE induced contraction than that of KCl, suggesting involvement of $K^+$ channel in the relaxant effect. Both glibenclamide$(10^{-5}M)$, a $K_{ATP}$ channel inhibitor and indometacin, a cyclooxygenase inhibitor, completely prevented this relaxation. The relaxation effects of JGH, involve in part the release of nitric oxide from the endothelium as pretreatment with L-NAME, an NOS inhibitor, and methylene blue, a cGMP inhibitor, attenuated the responses by 62% and 58%, respectively. In addition, nitrite was produced by JGH in human aortic smooth muscle cells and human umbilical vein endothelial cells. The relaxant effect of JGH was also inhibited by 55.41% by tetraethylammonium(TEA; 5mM), a $K_{Ca}$ channel inhibitor. In the absence of extracellular $Ca^{2+}$, pre-incubation of the aortic rings with JGH significantly reduced the contraction by PE, suggesting that the relaxant action of the JGH includes inhibition of $Ca^{2+}$ release from intracellular stores. These results indicate that in rat thoracic aorta, JGH may induce vasodilation through ATP sensitive $K^+$ channel activation by prostacyclin production. However, the relaxant effect of JGH may also mediated in part by NO pathways and $Ca^{2+}$ activated $K^+$ channel.

Keywords

References

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