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. Author manuscript; available in PMC: 2017 Dec 1.
Published in final edited form as: Hypertension. 2016 Oct 3;68(6):1483–1493. doi: 10.1161/HYPERTENSIONAHA.116.07747

Figure 1. AngII-driven presympathetic PVN neuronal activity and sympathoexcitatory output requires functional glutamate receptors.

Figure 1

A, Bath-applied AngII (0.5 μM) increases the firing activity of a presympathetic PVN neuron, an effect blocked by glutamate receptor antagonism. B, Representative segments of firing activity for each recording condition in A are shown at an expanded time scale. C, Summary data showing mean firing activity in each recording condition (n=13). D, Summary data showing mean percent changes in renal sympathetic nerve activity (RSNA) evoked by AngII (0.2 nmol) in control conditions, or in the presence of the NMDA receptor blocker AP5 (2 nmol, n=5). *P< 0.05