가토 신동맥의 고농도 Histamine에 의한 노아드레날린 유발 수축 및 K-경축 약화 기전

Effects of Histamine Pretreatment on the subsequent Noradrenaline-induced Contraction and K⁺-Contracture in Rabbit Renal Artery

The contraction of renal arterial strip by no.epineph.me (NE) or 40 mM K⁺ were Significantly attenuated after histamine (10^-5 M)-induced contraction. The mechanisms of this phenomenon were investigated in the helical strips of isolated renal artery with the measurement of isometric tension. The arterial strip was immersed in the tris-buffered Tyrode s solution which was equilibrated with 100% O₂ at 35℃. The contraction was induced by NE or 40 mM K⁺ during the recovery from the histamine-induced contraction which lasted for 15 minutes. The contraction by NE was also attenuated in the Ca²⁺-free Tyrode s solution and the increase of contraction by addition of 2 mM Ca²⁺ was attenuated as well. This attenuation phenomenon was not observed in the presence of low concentration (3 X 10^-7 M) of histamine. This attenuation was not affected by destruction of endothelium, pretreatment with papaverine or propranolol. This attenuation was partially inhibited by pretreatment of ouabain or in low K⁺(0.5 mM) Tyrode s solution. But the attenuation in the Ca²⁺-free Tyrode s solution was not inhibited. Furthermore this attenuation was completely blocked by pretreatment of djphenhydramine (H₁-receptor blocker) and potentiated by pretreatment of cimetidine (H₂-receptor blocker). This attenuation Phenomenon was disappeared after recovery of 1 hour. From the above results, it is suggested that the attenuation phenomenon may be resulted partially from the activation of Na⁺-K⁺ exchange pump and partially from the depletion of intracellular Ca²⁺ pool after the histamine-induced contraction mediated through H₁-receptor function.