Effect of lithium on endothelial-dependent relaxation to melatonin in rat aorta

흰쥐 대동맥에서 melatonin의 내피 의존적 혈관 이완 작용에 대한 lithium의 영향

  • Kim, Shang-Jin (Bio-Safety Research Institute, Chonbuk National University) ;
  • Yu, Xianfeng (Bio-Safety Research Institute, Chonbuk National University) ;
  • Cho, In-Gook (Bio-Safety Research Institute, Chonbuk National University) ;
  • Kang, Hyung-Sub (Bio-Safety Research Institute, Chonbuk National University) ;
  • Kim, Jin-Shang (Bio-Safety Research Institute, Chonbuk National University)
  • 김상진 (전북대학교 생체안전성연구소) ;
  • 유선봉 (전북대학교 생체안전성연구소) ;
  • 조인국 (전북대학교 생체안전성연구소) ;
  • 강형섭 (전북대학교 생체안전성연구소) ;
  • 김진상 (전북대학교 생체안전성연구소)
  • Accepted : 2005.11.22
  • Published : 2005.12.29

Abstract

Melatonin, the principal hormone of the vertebral pineal gland, participates in the regulation of cardiovascular system in vitro and in vivo. Lithium inhibits both inositol polyphosphate phosphatase (IPPase) and inositol monophosphatase (IMPase), which are involved in a wide range of signal transduction pathways. The aim of the present study was to assess the effect of lithium on endothelial-dependent relaxation to melatonin and on the melatonin-induced inhibition of contraction by phenylephrine (PE) in isolated rat aorta. Melatonin induced a concentration-dependent relaxation in PE-precontracted in endothelium-intact (+E) aortic rings. Melatonin inhibited a PE-induced sustained contraction in +E aortic rings. These effects of melatonin on relaxation and contractile responses were inhibited by pretreatment with lithium. In PE-precontracted +E aortic rings, the melatonin-induced vasorelaxations and the inhibitory effects of melatonin on maximal contractions were inhibited by endothelium removal or by pretreatment with L-$N^G$-nitro-arginine (L-NNA), 1H-[1,2,4] oxadiazolo-[4,3-a] quinoxalin-1-one (ODQ) and nifedipine and verapamil, but not by tetrabutylammonium, clotrimazole and glibenclamide, However, in endothelium-denuded (-E) aortic rings and in the presence of L-NNA and ODQ in +E aortic rings, the melatonin-induced residual relaxations and the melatonin-induced residual contractile responses to PE were not affected by lithium. It is concluded that the inositol phosphate pathway may be involved in endothelial-dependent relaxation induced by melatonin.

Keywords

References

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