1 We have studied the contractile effects of noradrenaline and neuropeptide Y given alone and in combination on isolated rat renal interlobar arteries. 2 Noradrenaline contracted proximal and distal intrarenal microvessels in a concentration dependent manner, with similar potency (EC50≈ 550 nM), but maximum effects were greater in the proximal than in the distal vessel segments (≈ 10 and 6 mN, respectively). 3 The noradrenaline‐induced contraction was inhibited by low prazosin concentrations (3‐‐10 nM) but not by 1 μM yohimbine indicating involvement of α1‐ but not α2‐adrenoceptors. The α1A‐adrenoceptor‐selective antagonists, 5‐methylurapidil and tamsulosin, had high potency (apparent affinities of ≈ 8 nM and 57 pM, respectively) while the α1D‐adrenoceptor‐selective antagonist, BMY 7378, had only low potency (apparent affinity ≈ 300 nM). The α1B‐adrenoceptor‐alkylating agent, chloroethylclonidine (10 μM for 30 min at 37°C), had no inhibitory effects. The Ca2+ entry blocker, nitrendipine (300 nM), reduced the potency and maximal effects of noradrenaline. 4 Neuropeptide Y (1‐‐100 nM) also contracted interlobar arteries in a concentration dependent manner, with greater effects in the proximal than in the distal segments, but maximal effects were only small in either segment (50 but this enhancement was also small. 5 We conclude that noradrenaline contracts rat interlobar arteries by an α1A‐adrenoceptor; its co‐transmitter, neuropeptide Y, affects the response only marginally in this vascular bed.