Figure 4. TRPA1 mediates the vasodilator component of cold-induced responses.

Blood flow was measured using FLPI in anaesthetized mice following immersion of the ipsilateral hindpaw in cold (10 °C) water and the contralateral hindpaw remained untreated. (a) Representative blood flow trace of a cold-induced vascular response and (b) restoration of cutaneous blood flow, as assessed by AUC for 30 min following cold water immersion in WT mice pretreated with the TRPA1 antagonist HC030031 (6 mg kg⁻¹, i.v., n=6) or control (8% DMSO in 2% Tween-80 in saline, n=6) at the maximum vasoconstriction phase following local cold water immersion. (c) % Maximum change in hindpaw blood flow from baseline to 0–2 min following local cold treatment (maximum vasoconstriction), (d) Representative blood flow trace of a cold-induced vascular response and (e) Restoration of cutaneous blood flow, as assessed by AUC for 30 min following cold water immersion in WT mice pretreated with the TRPV1 agonist resiniferatoxin (0.3 mg kg⁻¹, s.c. daily., 4 days, n=8) or control (10% ethanol, 10% Tween-80 in saline, s.c. daily, 4 days, n=9). (f) Representative blood flow trace of a cold-induced vascular response, (g) % Maximum change in hindpaw blood flow from baseline to 0–2 min following local cold treatment (maximum vasoconstriction) and (h) Restoration of cutaneous blood flow, as assessed by AUC for 30 min following cold water immersion in WT mice pretreated with the CGRP receptor antagonist BIBN4096 (0.3 mg kg⁻¹, i.v., 5 min, n=9) or control (saline, i.v., 5 min, n=10). All error bars indicate s.e.m. *P<0.05, **P<0.01, ***P<0.001 versus respective untreated, ^##P<0.01, ^###P<0.001 versus cold-treated hindpaw (analysis of variance, Bonferroni post hoc test).