Current evidence suggests that the most parsimonious mechanism for functional activity of gabapentinoid drugs is their binding to the auxiliary α2δ subunit of voltage-dependent calcium channels (VDCCs) and subsequent functional modulation of these channels. Auxiliary α2δ subunit of VDCCs was identified as a critical component of increased calcium currents in arterial myocytes of SHR. This presentation will focus on our study investigating the hemodynamic response to gabapentin in conscious spontaneously hypertensive rats.