2K1C is a model of renovascular hypertension with an exaggerated intracellular calcium (Ca²⁺_i) response to angiotensin II (ANG II) in isolated afferent arterioles (AAs) from the clipped kidney. To explore the role of NO release in this model, we studied ANG II (10^-7 mol/L) induced calcium signalling and contractility with L-NAME. In AAs from the non-clipped kidney, L-NAME increased the ANG II induced Ca²⁺_i response from 0.280.05 to 0.550.09 (Fura-II 340 nm/380 nm ratio), and increased contraction from 806 % of baseline to 606 % of baseline (p < 0.05). In vessels from sham and clipped kidneys, L-NAME had no effect. In DAF-FM loaded AAs from the non- clipped kidney, ANG II increased NO-derived fluorescence to 14534 % of baseline (p < 0.05 vs. sham), but not in sham or clipped kidney vessels. In the non-clipped kidney, cationic aminoacid transferase (CAT) 1 and 2 mRNA was increased in both kidneys from 2K1C (p < 0.05), indicating an increased transport-capacity of the NO precursor L-arginine. To pursue the role of ANG II, we used ANG II infused rats using Alzet micropumps for 14 days. Ten animals from each group received the AngII AT1 receptor blocker Losartan in the drinking water. mRNA expression was investigated for the genes for eNOS, CAT-1, CAT-2, DDAH-1, DDAH-2, Arginase-1 and Arginase-2 using real time reverse transcriptase PCR. 18S RNA was used as internal control. eNOS, DDAH-1 and Arginase-2 were not changed by ANG II infusion and were not affected by Losartan treatment. CAT-2, DDAH-2 and Arginase-1 were significantly increased in AngII infused rats and the expressions were blunted by Losartan treatment. In conclusion, the mRNA expressions of CAT-2, DDAH-2 and Arginase-1 AAs seem to be regulated by AT1 receptor dependant mechanism.