The contractile mechanisms of serotonin were investigated in the renal artery of a rabbit. The helical strips of isolated renal artery were immersed in the normal or Ca²⁺-free tris-buffered Tyrode s solution, which was equilibrated with 100% O₂ at 35℃. The contraction by serotonin or norepinephrine (NE) began at 1 X 10^-7 M and reached the maximal contraction at 1 X 10^-5 M. The maximal contraction by serotonin corresponded to 58.1±4.2% of maximal contraction by NE. Cyproheptadine, a serotonin receptor blocker, shifted the concentration-response curve to the right without any reduction in the maximum response but shifted that of NE to the right with reduction in maximum response. And phentolamine, an α-receptor blocker, shifted the concentration-response curve of serotonin or NE without any reduction in maximum responses. The pA₂ values for cyproheptadine against serotonin and NE were 10.35±0.04 and 8.45±0.13, respectively. The pA₂ values for phentolamine against serotonin and NE were 6.87±0.04 and 8.14±0.08, respectively. after the pretreatment with 6-hydroxydopamine, the contraction induced by 100 mM K⁺, tyramine and serotonin reduced to 83.0±2.0, 26.8±6.2 and 82.0±3.5% of control, respectively. The contraction by serotonin in the Ca²⁺-free Tyrode s solution was increased and sustained with the addition of Ca²⁺ extracellulary. The serotonin-sensitive intracellular Ca²⁺ pool was depleted completely by the pretreatment with NE, but the NE-sensitive intracellular Ca²⁺ pool was depleted partially by the pretreatment with serotonin. From the above results, it is suggested that the contraction induced by serotonin in the renal artery of a rabbit may be due to mechanisms in which serotonin acts directly on specific serotonin receptors and also acts indirectly on α-adrenoceptors by displacing NE from neuronal stores.