Abstract
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% $O_2\;at\;35^{\circ}C$. 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 $Ca^{2+}-free$ Tyrode's solution and the increase of contraction by addition of 2 mM $Ca^{2+}$ was attenuated as well. This attenuation phenomenon was not observed in the presence of low concentration $(3{\times}10^{-7}\;M)$ 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 $Ca^{2+}-free$ Tyrode's solution was not inhibited. Furthermore this attenuation was completely blocked by pretreatment of djphenhydramine $(H_1-receptor blocker)$ and potentiated by pretreatment of cimetidine $(H_2-receptor\;blocker)$. 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 $Ca^{2+}$ pool after the histamine-induced contraction mediated through $H_1-receptor$ function.