Background and purpose:Experiments were designed to determine the modulation by nitric oxide (NO) and endothelium‐dependent hyperpolarizations (EDHF‐mediated responses) of endothelium‐dependent contractions in renal arteries of normotensive and hypertensive rats.Experimental approach:Rings, with or without endothelium, of renal arteries of 8‐month‐old Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were suspended in myographs for isometric force recording.Key results:ACh evoked relaxations in preparations contracted with phenylephrine. L‐NAME (inhibitor of NOS) attenuated (WKY) or abolished (SHR) these relaxations. TRAM‐34 plus UCL 1684 (inhibitors of EDHF‐mediated responses) did not decrease the relaxation, except in rings of WKY when L‐NAME was also present. High concentrations of ACh caused a secondary increase in tension, augmented in rings of WKY by L‐NAME or TRAM‐34 plus UCL 1684. The increase in tension was prevented by indomethacin. Under baseline tension, ACh induced endothelium‐dependent contractions, prevented by indomethacin (COX inhibitor) or terutroban (TP receptor antagonist). The calculated endothelium‐dependent contractions were larger in rings of SHR compared with those of WKY. In preparations of SHR, the contractions were augmented by L‐NAME in the presence of SC19220 (EP‐1 receptor antagonist). In arteries of WKY, the endothelium‐dependent contractions were augmented by TRAM‐34 plus UCL 1684. The responses were reduced by SC19220.Conclusions and implications:In the renal artery of the rat, EDCF‐mediated contractions are augmented by hypertension. The endothelium‐dependent contractions are facilitated by NOS inhibition (in the presence of an EP‐1 receptor antagonist) and by the withdrawal of EDHF‐mediated responses.British Journal of Pharmacology (2008) 155, 217–226; doi:10.1038/bjp.2008.256; published online 23 June 2008