Aim To investigate the mechanism of the change in the reactivity of the remodeling vessels of hypertension to Angiotensin Ⅱ(AngⅡ). Methods Use the method of Video-Microscope to observe the contractility of the third embranchment of the mesentery artery of the normotensive Sprague-Dawley (SD) rats and the two-kideny one-clip (2K1C) renal hypertension(RH) rats to AngⅡ. Use the method of isolation vascular ring perfusion to exploration the activity to AngⅡ of the aortic rings either group rats and the effect of losartan on the actibity. Use RT-PCR to measure AT1R mRNA and AT2R mRNA expression in the thoracic aorta of either group rats. Results All of the contractility of the aortic rings and the third embranchment of the mesentery artery to AngⅡ increased with dose-dependented, and the constractility of the remodeling vessels of the 2K1C RH rats to AngⅡ toned up more evidently at every dose of angiotensionⅡ. Loarstan block the the contractility of the aortic rings to AngⅡ completely. AT1R mRNA expression in the thoracic aorta of 2K1C RH rats is more than which in the the thoracic aorta of normotensive rats and AT2R mRNA express only in the thoracic aorta of 2K1C RH rats. Conclusions (1) The response of the remodeling vessel in hypertension to AngⅡtone up . (2) The mechanism of change in the reactivity of remodeling vessel of renal hypertension rats to Angiotensin Ⅱ may due to AT1R mRNA up-regulated.