
This study determined whether prolonged treatment with the calcineurin inhibitor causes elevated sympathetic output and persistent hypertension by potentiating synaptic N-methyl-D-aspartate (NMDA) receptor activity in the PVN. Immunocytochemistry labelling showed that calcineurin was expressed in parasympathetic neurons in the PVN. Also, treatment with FK506 markedly increased PVN parasympathetic neurons' presynaptic and postsynaptic NMDA receptor activity. The findings reveal that normal calcineurin activity in the PVN constitutively restricts sympathetic vasomotor tone via suppressing NMDA receptor activity, which may be targeted for treating calcineurin inhibitor-induced hypertension.
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