A growing body of evidence supports an elevated NMDA receptor‐mediated glutamate excitatory function in the SON and PVN of hypertensive rats that contributes to neurohumoral activation in this disease. Still, the precise mechanisms underlying altered NMDAR signalling in hypertension remains to be elucidated. In this study, we performed simultaneous electrophysiology and fast confocal Ca2+ imaging to determine whether an altered NMDAR‐mediated changes in intracellular Ca2+ levels (NMDAR‐ΔCa2+) occurred in hypothalamic magnocellular neurosecretory cells (MNCs) in renovascular hypertensive (RVH) rats. We found that despite evoking a similar excitatory inward current, activation of NMDARs resulted in a larger and prolonged ΔCa2+ in MNCs from RVH rats. Changes in NMDAR‐ΔCa2+ dynamics were observed both in somatic and dendritic compartments. Inhibition of the ER SERCA pump activity with thapsigargin prolonged NMDAR‐ΔCa2+ responses in MNCs of sham rats, but this effect was occluded in RVH rats, thus equalizing the magnitude and time course of the NMDA‐ΔCa2 responses between the two experimental groups. Taken together, our results support (1) an exacerbated NMDAR‐ΔCa2+ response in somatodendritic compartments of MNCs of RVH rats, and (2) that a blunted ER Ca2+ buffering capacity contributes to the altered NMDAR‐ΔCa2+ dynamics in this condition. Thus, an altered spatiotemporal dynamics of NMDAR‐ΔCa2+ response stands as an underlying mechanisms contributing to neurohumoral activation in neurogenic hypertension. This article is protected by copyright. All rights reserved