Muscle metabolic by‐products stimulate thin fiber muscle afferent nerves and evoke reflex increases in sympathetic nerve activity (SNA) and blood pressure (BP). It has been reported that metabolically sensitive transient receptor potential cation channel subfamily A, member 1 (TRPA1) appears on sensory afferent neurons and plays a role in regulating SNA and BP responses evoked by muscle contraction. The responses of sensory nerves (neurons) to muscle metabolites are altered under the conditions of insufficient limb blood supply in peripheral artery disease (PAD), induced by femoral artery ligation in rats. In turn, SNA and BP responses are exaggerated by an ischemic insult to the muscle. Our data show that 1) TRPA1 is expressed in C‐fiber of DRG neurons; 2) femoral occlusion increases the protein levels of TRPA1 in the dorsal root ganglion (DRG) (optical density: 0.97 ± 0.02 in control; and 1.68 ± 0.03 after ischemia, P < 0.05 vs. control; n = 6 in each group); and 3) renal SNA and mean BP responses to AITC (40μg/kg, a TRPA1 agonist) are also enhanced after chronic ischemia (61±5%, 31±5 mmHg in controls; and 89±8%, 44±3 mmHg after ischemia, P<0.05 vs. control, n=14 in each group). Thus, alternations in sensory nerves'TRPA1 likely contribute to enhanced sympathetically mediated cardiovascular responses under circumstances of chronic muscle ischemia observed in PAD patients. (Supported by NIH P01 HL096570 & AHA EIA 0840130N)