흰쥐 대동맥 수축에 대한 xylamine의 억제효과

Inhibitory effects of xylamine on the arterial contraction in rats

  • 김상진 (전북대학교 생체안전성연구소) ;
  • 강형섭 (전북대학교 생체안전성연구소) ;
  • 김진상 (전북대학교 생체안전성연구소)
  • Kim, Sang-Jin (Department of Pharmacology, College of Veterinary Medicine, Chonbuk National University) ;
  • Kang, Hyung-sub (Department of Pharmacology, College of Veterinary Medicine, Chonbuk National University) ;
  • Kim, Jin-shang (Department of Pharmacology, College of Veterinary Medicine, Chonbuk National University)
  • 심사 : 2004.05.28
  • 발행 : 2004.09.30

초록

The therapeutic efficacy of xylamine in the field of psychological medicine has been recognized for years and the drug is used to treat depression and some other conditions, but little is known about its mechanism of action on vascular system. Therefore, the present study was designed to investigate the influence of xylamine on the contractile responses of isolated rat thoracic arteries to phenylephrine(PE) and potassium chloride(KCl). Xylamine produced a concentration-dependent relaxation in PE-precontracted endothelium intact(+E) rat aortic rings, but not in a KCl-precontracted aortic rings. Also, xylamine inhibited the PE-induced contraction in concentration-dependent manner, but not in the high KCl-induced contraction in +E rings. This concentration-dependent inhibition was suppressed by the removal of the endothelium (-E). The inhibitory effects of xylamine($0.3{\mu}M$) on the PE-induced contractions were suppressed by N(G)-nitro-L-arginine(L-NNA), N(omega)-nitro-L-arginine methyl ester(L-NAME), aminoguanidine, dexamethasone, methylene blue, 1H-[1,2,4]oxadiazolo [4,3-a]quinoxalin-1-one(ODQ), indomethacin, ryanodine, tetrabutylammonium(TBA), lidocaine, procaine and 0 mM extracellular $Na^+$, but not by 2-nitro-4-carboxyphenyl-n,n-diphenylcarbamate(NCDC), lithium, nifedipine, verapamil, 0 mM extracellular $Ca^{2+}$, glibenclamide and clotrimazole. These findings suggest that xylamine could act as a vasorelaxant and direct inhibitor of arterial contraction. This vasorelaxation involves an endothelial nitric oxide (NO)/cGMP (guanosine 3',5'-cyclic monophosphate) pathway or cyclooxygenase system, and an interference with $Ca^{2+}$ release, TBA-sensitive $Ca^{2+}$-activated $K^+$ channels and $Na^+$$ channels.

키워드

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