We hypothesized that AT₂ receptor (AT₂R) inhibits renal renin biosynthesis in young rats via NO. We monitored changes in renal NO, cGMP, renin content (RRC) and angiotensin II (Ang II) in 4 wk old rats in response to low sodium (LNa⁺) intake alone and combined with 8 h direct renal cortical administration of AT₁ receptor blocker valsartan (VAL), AT₂R blocker PD123319 (PD), NO synthase inhibitor L-NAME, NO donor SNAP or guanylyl cyclase inhibitor ODQ. In addition we monitored renal eNOS and nNOS in response to VAL or PD. LNa⁺, VAL, PD, L-NAME and ODQ increased RRC, Ang II, and renin mRNA. PD and L-NAME decreased NO and cGMP while SNAP reduced RRC, Ang II, renin mRNA and reversed the effects of PD. PD also reduced eNOS and nNOS protein and mRNA. Combined treatment with PD, L-NAME or ODQ and VAL reversed the effects of VAL and caused further increase in RRC, Ang II, renin mRNA and protein. ODQ reversed the effects of SNAP. These data demonstrate that the renal AT₂ receptor decreases renal renin biosynthesis and Ang II production in young rats. Reversal of the PD effects by SNAP and SNAP effects by ODQ confirms that NO and cGMP mediate the AT₂ receptor inhibition of renal renin production.