To examine the role of the purinergic and noradrenergic components in the potentiation of endothelin‐1 on the vascular response to sympathetic nerve stimulation, we recorded the isometric response of isolated segments, 2 mm long, from the rabbit central ear artery to electrical field stimulation (1–8 Hz) under different conditions, at 37°C and during cooling (30°C). Electrical field stimulation produced frequency‐dependent contraction, which was reduced during cooling (about 60% for 8 Hz). Both at 37°C and 30°C, phentolamine (1 μ M ) or blockade of α 1 ‐adrenoceptors with prazosin (1 μ M ) reduced, whereas blockade of α 2 ‐adrenoceptors with yohimbine (1 μ M ) increased, the contraction to electrical field stimulation. This contraction was increased after desensitization of P2‐receptors with α,β‐methylene adenosine 5′‐triphosphate (α,β‐meATP, 3 μ M ) at 37°C but not at 30°C, and was not modified by blockade of P2‐receptors with pyridoxalphosphate‐6‐azophenyl‐2,4′‐disulphonic acid (PPADS, 30 μ M ) at either temperature. Endothelin‐1 (1, 3 and 10 n M ) at 37°C did not affect, but at 30°C it potentiated in a concentration‐dependent manner the contraction to electrical field stimulation (from 28±6 to 134±22%, for 8 Hz). At 37°C, endothelin‐1 in the presence of phentolamine or prazosin, but not in that of yohimbine, α,β‐meATP or PPADS, potentiated the contraction to electrical stimulation. At 30°C, phentolamine or yohimbine reduced, prazosin or PPADS did not modify and α,β‐meATP slightly increased the potentiation by endothelin‐1 of the response to electrical stimulation. The arterial contraction to ATP (2 m M ) and the α 2 ‐adrenoceptor agonist BHT‐920 (10 μ M ), but not that to (−)‐noradrenaline (1 μ M ), was potentiated by endothelin‐1 at both 37°C and 30°C. These results in the rabbit central ear artery suggest that the sympathetic response: (a) at 37°C, could be mediated mainly by activation of α 1 ‐adrenoceptors, with low participation of P2‐receptors, (b) is diminished during cooling, probably by a reduction in the participation of α 1 ‐adrenoceptors, and in this condition the response could be mediated in part by P2‐receptors, and (c) is potentiated by endothelin‐1 during cooling, probably by increasing the response of both postjunctional α 2 ‐adrenoceptors and P2‐receptors. British Journal of Pharmacology (1997) 122 , 172–178; doi: 10.1038/sj.bjp.0701359