Renal afferent neurons exhibit predominantly tonic firing pattern upon depolarizing current injection, most likely due to specific expression of voltage gated sodium channels. We recently could show in an in vitro model that inflammation alters firing activity. However, the role of these neurons in vivo is unclear.With this study we aim to investigate the firing patterns of renal afferent neurons in a model of hypertension.

Clipping of the renal artery induced hypertension in male Sprague-Dawley rats (n=4). DiI-labeling allowed the identification of dorsal root ganglion (DRG) neurons (Th11-L2) with projections to the kidney. Current clamp was used to characterize neurons according to their firing response upon stimulation as “tonic”, i.e. sustained action potential (AP) firing or as “phasic”,i.e. showing <5 APs. Firing threshold, overshoot and AP- duration were determined in renal neurons of hypertensive animals and compared those of sham-operated controls (n=4).

Renal DRG neurons of hypertensive animals (n=92) show a significant decrease of tonic firing pattern (41, 3% vs. 61,7%) compared to controls(n=81). Interestingly, neither tonic nor phasic neurons exhibited significant changes in action potential shape e.g. overshoot, firing threshold and AP- duration in hypertensive animals; cell parameters (capacity, resistances) were equal in both groups.

In conclusion we found that renal afferent DRG neurons exhibit significantly less tonic firing pattern in neurons from hypertensive animals. The underlying mechanisms need further elucidation. However, as these findings are similar to our former results in inflammation, modulation of the voltage gated sodium channels could be a possible mechanism.