Agonist drugs of the serotonin 2A receptor (psychedelics) are used with functional magnetic resonance imaging (fMRI) to investigate the neural correlates of conscious perception. A significant limitation is the indirect nature of the fMRI signal, which reflects changes in blood flow. It is therefore crucial to distinguish neuronal activity from confounding vascular effects of the drugs themselves. We investigated the hemodynamic response associated with the acute state induced by three serotonergic psychedelics (LSD, psilocybin, and DMT) using deconvolution algorithms applied to resting-state fMRI. We estimated the hemodynamic response function (HRF) under both drug and placebo conditions, finding significant global and regional changes in HRF latency. This suggests a serotonergic alteration in neurovascular coupling. To investigate the mechanisms, we implemented biophysical models based on mean-field descriptions of neuronal activity coupled through the structural connectome. Modeling neurovascular coupling produced interpretable parameters related to vascular biomechanics, supporting the hypothesis that observed fMRI changes under psychedelics could be partially explained by non-neuronal factors linked to vasoconstriction and dilation.