•  The autoregulatory capacity of the cerebral vasculature allows for maintenance of relatively stable blood flow in the face of fluctuating arterial pressure to protect neural tissue from wide swings in oxygen and nutrient delivery. •  We recently found that neurogenic control plays an active role in autoregulation. Although myogenic pathways have also been hypothesized to play a role, previous data have not provided an unequivocal answer. •  We examined cerebral blood flow responses to augmented arterial pressure oscillations with and without calcium channel blockade, and characterized autoregulation via a robust non‐linear method. •  Blockade significantly altered the non‐linearity between pressure and flow, particularly at the slowest fluctuations, and the same rate of change in pressure elicited a larger change in flow than at baseline. •  These results show that myogenic mechanisms also play a significant role in cerebrovascular regulation, and help us better understand physiological mechanisms that underlie cerebral autoregulation in humans. Abstract  Although myogenic mechanisms have been hypothesized to play a role in cerebrovascular regulation, previous data from both animals and humans have not provided an unequivocal answer. However, cerebral autoregulation is explicitly non‐linear and most prior work relied on simple linear approaches for assessment, potentially missing important changes in autoregulatory characteristics. Therefore, we examined cerebral blood flow responses to augmented arterial pressure oscillations with and without calcium channel blockade (nicardipine) during blood pressure fluctuations (oscillatory lower body negative pressure, OLBNP) across a range of frequencies in 16 healthy subjects. Autoregulation was characterized via a robust non‐linear method (projection pursuit regression, PPR). Blockade resulted in significant tachycardia, a modest but significant elevation in mean arterial pressure, and reductions in mean cerebral blood flow and end‐tidal CO2 during OLBNP. The reductions in flow were directly related to the reductions in CO2 (r= 0.57). While linear cross‐spectral analysis showed that the relationship between pressure–flow fluctuations was preserved after blockade, PPR showed that blockade significantly altered the non‐linearity between pressure and flow, particularly at the slowest fluctuations. At 0.03 Hz, blockade reduced the range of pressure fluctuations that can be buffered (7.5 ± 1.0 vs. 3.7 ± 0.8 mmHg) while increasing the autoregulatory slope (0.10 ± 0.05 vs. 0.24 ± 0.08 cm s−1 mmHg−1). Furthermore, the same rate of change in pressure elicited a change in flow more than twice as large as at baseline. Thus, our results show that myogenic mechanisms play a significant role in cerebrovascular regulation but this may not be appreciated without adequately characterizing the non‐linearities inherent in cerebrovascular regulation.