The intrarenal renin-angiotensin system (RAS) has an important role in generating and maintaining hypertension in 2-kidney 1-clip (2K1C) rats. This study evaluated how various intrarenal RAS components contributed to hypertension not only in maintenance time (5w; 5 week after operation) but also in early time (2w; 2week after operation). We inserted a 2.5mm-sized clip into the left renal artery of the Sprague-Dawley rats and sacrificed them at 2w and 5w following operation. Systolic blood pressure increased within one week after operation and left ventricular hypertrophy was occurred in 2K1C rats. At 2w, juxtaglomerular apparatus (JGA) and collecting duct (CD) renin increased in CK. The tubular angiotensin I-converting enzyme (ACE) was not changed, but peritubular ACE2 decreased in NCK and CK. At 5w, ACE and CD rein were enhanced, and ACE2 was still lessened in both kidneys of 2K1C rat. However, plasma renin activity (PRA) was not different with that of sham rat. In proximal tubule of CK, AngII type 1 receptor (AT1R) was not suppressed, but Mas receptor (MasR) was reduced; thus, the AT1R/MasR ratio was elevated. Although hypoxic change of CK could not be excluded, the JGA renin of CK and CD renin of both kidneys was highly expressed independent of time. Peritubular ACE2 changed in early time and uninhibited AT1R in proximal tubule of CK was presented in maintenance time. In 2K1C rat, attenuated ACE2 seems to contribute to initiating hypertension while up-regulated ACE in combination with un-suppressed AT1R may have a key role in maintaining hypertension.