Cold stress (CS), triggers significant autonomic and hemodynamic disturbances, mediated in part by transient receptor potential (TRP) channels. This study investigates the distinct contributions of TRPM8 and TRPV1 in autonomic cardiovascular regulation during CS. Conscious male Sprague-Dawley rats were administered AMTB (TRPM8 antagonist) or capsazepine (CPZ; TRPV1 antagonist), while controls received either normal saline (NS) or dimethyl sulfoxide (DMSO). Hemodynamic parameters, including systolic blood pressure (SBP), heart rate (HR), and core temperature (ToC), were continuously monitored. Spectral analyses of blood pressure variability (BPV), and heart rate variability (HRV), were used to assess autonomic modulation. AMTB administration led to ToC declines and altered sympathetic activity, while CPZ attenuated cold-induced pressor (CIP) and tachycardic (CIT) responses, improved baroreflex sensitivity, and shifted autonomic balance toward parasympathetic dominance. The findings highlight TRPM8’s role in sensory-driven thermoregulation and TRPV1’s broader function in baroreflex and autonomic stability. This study provides novel insights into the interplay between TRPM8 and TRPV1 in somato-sympathetic reflex modulation and suggests potential therapeutic applications for managing cold-induced cardiovascular dysfunctions. Highlights TRPM8 and TRPV1 modulate pain and autonomic responses during cold stress. Cold exposure triggers nociceptors and cardiovascular autonomic reflexes. Spectral analysis reveals effects of TRPM8 and TRPV1 antagonists on cold stress. Both antagonists attenuate pressor responses and blood pressure variability.