The aims of this study were to develop a technique to measure blood flow in the mouse ear and to investigate the nature of the vasodilator mediator(s) involved in the response to capsaicin. The response to capsaicin, applied topically, was investigated in anaesthetized CD1 or Sv129+C57BL/6 wild‐type (+/+) or NK1 receptor knockout mice (−/−). Blood flow was assessed by laser Doppler flowmetry and oedema formation by 125I‐albumin accumulation. Capsaicin induced significant increases in blood flow (0.2–200 μg in 20 μl) and oedema (2–200 μg in 20 μl). The oedema response was absent in NK1−/− mice and NK1+/+mice treated with the selective NK1 receptor antagonist SR140333 (480 nmol kg−1) as expected. Furthermore, the capsaicin‐evoked increase in blood flow was significantly potentiated in the knockout mice (203% of wild‐type response, P<0.05) and wild‐type mice treated with SR140333 (201%, P<0.05). The CGRP receptor antagonist CGRP8–37 (400 nmol kg−1) had no effect on capsaicin‐induced blood flow in NK1+/+mice but abolished the increased blood flow to capsaicin in NK1−/−, and NK1+/+wild‐type mice pre‐treated with SR140333. The results indicate that neurogenic vasodilatation can be measured in the mouse ear. The capsaicin‐induced increased blood flow involves activation of, and possible interactions between, both NK1 and CGRP1 receptors. British Journal of Pharmacology (2002) 135, 356–362; doi:10.1038/sj.bjp.0704485