In rat tail artery, electrical stimulation of the sympathetic nerves evokes both an ATP-mediated excitatory junction potential (EJP) and a slower noradrenaline-mediated depolarization (NAD). Here we investigated the mechanisms underlying the NAD. Segments of proximal tail artery isolated from rats were mounted in a 1 ml recording chamber and the perivascular axons were electrically stimulated via a suction electrode applied to the proximal end. Intracellular recordings were made from the vascular smooth muscle cells. Application of the α₁-adrenceptor antagonist prazosin (0.1 μM, n = 6) slowed the rising phase of the NAD but did not change its amplitude or duration. In contrast, the α₂-adrenoceptor antagonist idazoxan (1 μM, n = 6) did not change the onset of the NAD but it did reduce its amplitude and duration. The combined application of prazosin and idazoxan abolished the NAD. In the presence of prazosin, the NAD was completely blocked by the K_ATP channel blockers, glybenclamide (10 μM, n = 6) and PNU 37883A (5 μM, n = 6). These agents also produced membrane depolarization. The NAD remaining when α₂-adrenoceptors were blocked was not affected by glybenclamide (10 μM, n = 5). In rat tail artery, the time constant of decay of the EJP is determined by the membrane time constant (Cassell et al., 1988). The time constant of decay of EJPs evoked at the peak of the idazoxan-resistant NAD was prolonged (relative change 1.16 ± 0.03, P < 0.01, n = 6) suggesting that the α₁-component of the depolarization is also mediated by closure of K⁺ channels. However, this component was not inhibited by broad-spectrum K⁺ channel blockers (tetraethylammonium, 4-aminopyridine, Ba²⁺). The idazoxan-resistant NAD was also unaffected by the Cl^– channel blockers, 9-anthracene carboxylic acid (100 μM, n = 4) and niflumic acid (10 μM, n = 3). These findings indicate that the NAD has two components; one which is due to activation of α₁-adrenoceptors and the other to activation of α₂-adrenoceptors. The α₂-adrenoceptor-mediated component is due to closure of K_ATP channels whereas α₁-adrenoceptor mediated component is most likely mediated by closure of another type of K⁺ channel.