Unilateral ureteral obstruction (UUO) is a clinical scenario that leads to obstructive nephropathy. UUO alters the expression of many mediators in the ipsilateral kidney. Renin-angiotensin system (RAS) is involved in UUO. Angiotensin II (Ang II) and angiotensin 1-7 (Ang 1-7) as the main arms of RAS influence kidney function which may alter by UUO. Ang II via Ang II receptor subtypes I (AT1R) reduces renal blood flow and glomerular filtration rate and induces oxidative stress, apoptosis as well as inflammation in renal tissue and contributes to renal fibrosis in UUO model. Also, Ang 1-7 receptor (MasR) and Ang II receptor subtype II (AT2R) may have a protective effect against UUO-induced renal injury. In addition, there is crosstalk among RAS with the main vasodilator factors (prostaglandins E2 and I2, bradykinin, atrial natriuretic factor, nitric oxide and adenosine) and the main vasoconstrictor factors (endothelin and vasopressin) in the ipsilateral kidney with UUO. In this review, the roles of the RAS on renal function and its interactions with the other factors in the kidney with UUO were discussed.