To investigate the endothelium dependent vascular reactivity of the systemic arterial and the pulmonary arterial system in acute renal hypertensive rats of 2-kidney, 1-ligation type (RHRs), acetylcholine (ACh)-induced vasodilation and depressor effects were evaluated in isolated arteries and in vivo, respectively, in the presence and absence of functional endothelium. ACh (10^-5 M) relaxed the intact thoracic aortas from RHRs and normotensive rats (NRs), but the effect was significantly smaller for those from RHRs (34 and 86%, respectively, p<0.01). ACh-induced vasodilation was completely abolished after removal of endothelial cell or pretreatment with EDRF inhibitors, L-NAME and MB, indicative of its dependence on intact endothelial or EDRF function. ACh also induced vasorelaxation of the intact pulmonary arteries from RHRs and NRs; however, unlike the effects on the thorcic aorta, no significant difference in amplitude was noted between two groups. ACh (0.1 ~ 10μg/kg, i.v.) reduced mean systemic arterial pressure in anesthetized RHRs and in NRs to the similar magnitude (% change: 39 and 46% at 10μg/kg, respectively) and these hypotensive effects were significantly decreased after pretreatment with L-NAME (30 mg/kg, i.v.). Deprssor effects of ACh on mean pulmonary arterial pressure were similar in RHRs and NRs with and without pretreatment of L-NAME. However, in both NRs and RHRs, the depressor effects of ACh on mean pulmonary arterial pressure were significantly reduced compared with those for mean systemic arterial pressure, and the increment of mean pulmonary arterial pressure noted after L-NAME (0.1μ100 mg/kg, i.v.) was significantly smaller than that for mean systemic arterial pressure. These results indicate that in RHRs the endothelial cell function was impaired, at least in part, in systemic arterial system, but not in pulmonary arterial system, and both ACh-evoked and basal release of EDRF was less in the pulmonary arterial system than in systemic arterial system of both NRs and RHRs.