Retrograde signaling does not mediate sodium excretion during dorsal column stimulation

Abstract

Prior work found an increase in renal sodium excretion in male spontaneously hypertensive rats (SHR) following dorsal spinal column stimulation (DCS) at the spinal segment of the left renal sensory nerves (T12–T13). General sympathetic tone, and renal blood flow were unaltered by DCS. The effects of dorsal rhizotomy on the DCS‐induced renal sodium excretion was investigated in male SHR. SHR were randomly assigned to one of the following groups: no‐stimulation (NS), stimulation (S), no stimulation + Rhizotomy (NS+R), and Stimulation + Rhizotomy (S+R). Stimulated rats received DCS during the 2nd of five 15‐min. collection periods. Blood pressure was measured via a carotid artery cannula, and urine was collected via a bladder cannula. A standard stimulation parameter of 66% of the motor threshold (0.2 msec duration and 50 Hz) was used. Urine sodium was analyzed using flame photometry. Sodium excretion was significantly elevated in periods 3 and 4 in the S group when compared with corresponding periods in the NS group. Sodium excretion was significantly elevated in period 5 in the S+R group when compared with the NS+R. There were no differences between the S+R and the S groups. The DSC‐induced increase in sodium excretion is independent of retrograde signaling in the renal nerves. This research was funded by a departmental grant, in the Department of the Biological Sciences, Minnesota State University, Mankato, MN