Compensatory role for spinal glutamate in the regulation of renal sympathetic nerve activity in Wistar rats fed a low Na + diet

Spinal V 1 and glutamate receptor mediated RSNA are sensitized by high dietary Na + intake. This study compared the RSNA responses to intrathecal (IT) vasopressin (AVP) and glutamate infusion between male Wistar rats fed a normal Na + (NNa + , 0.3%) or low Na + (LNa + , 0.03%) diet from weaning (4 weeks) to adulthood (11 weeks). Adult rats were anaesthetized (1ml IP chloralose/urethane) and instrumented with arterial and IV cannulae. The tip of the IT cannula was placed at spinal vertebra T13. RSNA was recorded from the left kidney. ?RSNA (%baseline) were measured after IT AVP (1, 5, 10, 20 μM; 10 μL/2min; NNa + =6, LNa + =4) or glutamate (10, 20, 50, 100mM; 10 μL/2min, NNa + =6, LNa + =5). Data are presented as mean ± SE (% baseline RSNA). P<0.05 indicated significance. There was no difference in absolute baseline RSNA ( μV/s, NNa + 13±2, LNa + 17±6, P=0.21) or MAP (mmHg, NNa + 88±4, LNa + 92±3, P=0.36). IT AVP elicited a dose dependent rise in RSNA in NNa + , while RSNA responses were not observed at any dose of IT AVP in LNa + group (P<0.001). A dose dependent rise in RSNA to IT glutamate was observed in NNa + and LNa + . In addition, augmented RSNA responses were observed in LNa + at 10mM (NNa + : 98±1%, LNa + : 121±5%, P<0.01) and 50mM (NNa + : 109±2%, LNa + : 127±9% P<0.05). This suggests that LNa + intake blunts spinal AVP mediated RSNA, but the sympathoexcitatory pathway may be compensated by an increased sensitivity to spinal glutamate. Funding: HRB RP/2004/17.