Although only a small portion of patients with hypertension have renal hypertension, studies regarding renal hypertension may provide insight into the pathophysiology of essential hypertension. An increased vascular reactivity to vasoconstrictor substances has been observed both in clinical hypertension and in animal models of hypertension. This study was designed to evaluate the contractile and relaxing responses of the contralateral renal artery in renovascular hypertension and to provide an explanation of one of the mechanisms of renovascular hypertension. Methods : In the first experiment, an experimental renovascular hypertension model was established by clipping the left renal artery of Sprague-Dawley rats. These rats were then divided into two groups of which one was given enalapril during one week post-operation before being terminated. Ring preparations of the contralateral side of the renal artery were obtained one week after the operation. The contraction of renal artery strips were induced by high potassium or norepinephrine, and the relaxation of them were produced by acetylcholine or sodium nitroprusside. The contractile and relaxing responses were recorded and compared with the data obtained from control group. In the second experiment, the rats received angiotensin converting enzyme inhibitor, 5mg percent enalapril in the drinking water for 7 days after induction of renal artery stenosis operation. Then, the contractile and relaxing responses were evaluated by the same method as control group. Results : 1) The contralateral renal artery of renovascular hypertensive rats showed significantly increased contractile responses to the high potassium or norepinephrine as compared with that of control group (P<0.05). 2) Increased contractile reponses of the renal artery to the high potassium or norepinephrine were normalized to the control group level when enalapril was given. 3) The relaxing responses by acetylcholine were reduced on the contralateral renal artery in renovascular hypertensive rats as compared with that of the control group. However, no remarkable differences were noted between them with the sodium nitroprusside. 4) There were no significant differences in the acetylcholine or nitroprusside induced vasodilation response between enalapril-given renovascular hypertensive rats and control rats. Conclusion : These results suggest that endothelial dysfunctions may lead to renal hypertension and that enalapril(ACE inhibitor) may prevent the development of renal hypertension by maintaining endothelial function. (Korean. J. Med 57:925-932, 1999)