Fig. 4
Participation of TRPA1, SP and CGRP in cold-induced increases in blood flow in arthritic animals. a Percentage clearance of i.art. 99mTechnetium in the knee joint after 5 min in arthritic animals pretreated with selective TRPA1 antagonist, HC-030031 (100 mg/kg; i.p.), and exposed to cold (10 °C) for 1 h, n = 6. b Knee joint blood flow recorded using FLPI from arthritic animals pretreated with selective TRPA1 antagonist, HC-030031 (100 mg/kg; i.p.; 1 h), and exposed to cold (10 °C) for 1 h, n = 6–7, * p < 0.05 compared to vehicle-treated contralateral joint. c Knee joint blood flow recorded using FLPI from arthritic WT and TRPA1 KO mice exposed to cold (10 °C) for 1 h, n = 6–7, # p < 0.05 compared to WT CFA joint. d Knee joint blood flow recorded using FLPI in arthritic animals pretreated systemically with the selective NK1 antagonist SR140333 (480 mg/kg; i.v.; 15 min, n = 7) or the CGRP antagonist CGRP8–37 (400 mg/kg; i.v.; 15 min, n = 7), and exposed to cold (10 °C) for 1 h. For the vehicle-treated group, n = 13, * p < 0.05 compared to vehicle-treated ipsilateral joint. CFA complete Freund’s adjuvant, CGRP calcitonin gene-related peptide, FLPI full-field laser perfusion imager, KO knockout, NK 1 neurokinin 1, SP substance P, TRPA1 transient receptor potential ankyrin 1, WT wild-type