Frequency-Domain Analysis Links Autonomic Disruption to Renal Autoregulatory Failure after Spinal Cord Injury

Spinal cord injury (SCI) disrupts supraspinal autonomic pathways that regulate cardiovascular function, producing marked blood pressure instability and contributing to secondary injury in peripheral organs. The kidney is particularly vulnerable to these disturbances because renal blood flow (RBF) depends on tightly regulated interactions between neural, myogenic, and vascular control mechanisms. However, how SCI level and chronicity alter dynamic renal autoregulation remains poorly defined. Here, we investigated the effects of high- and low-thoracic SCI on renal hemodynamic control using in vivo blood pressure and RBF recordings in female mice. Hemodynamics were assessed at baseline and during acute sympathetic stimulation induced by norepinephrine (NE; 10 {micro}g/kg, i.v.) at 24 h and 4 wk following spinal cord transection at thoracic level 3 (T3) or thoracic level 10 (T10). Time-domain analyses quantified systolic blood pressure recovery, while frequency-domain analyses were used to resolve myogenic and sympathetic contributions to RBF regulation. High-thoracic SCI caused marked disruption of renal vascular responses to acute hypertension, producing paradoxical increases in RBF during NE-induced pressure elevations and sustained reductions in baseline and evoked RBF activity within frequency ranges associated with myogenic and sympathetic vasomotion. These impairments were most pronounced during the chronic phase of injury, consistent with loss of dynamic autoregulatory control and vascular remodeling. In contrast, low-thoracic SCI preserved baseline renal vasomotor activity and demonstrated recovery of dynamic autoregulatory responses over time. These findings identify SCI level and chronicity as critical determinants of renal microvascular regulation and demonstrate that high-thoracic SCI produces persistent autonomic-vascular uncoupling. This disruption of dynamic renal autoregulation represents a previously underappreciated mechanism of secondary organ vulnerability following neurotrauma. VISUAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=109 SRC="FIGDIR/small/735393v1_ufig1.gif" ALT="Figure 1"> View larger version (58K): org.highwire.dtl.DTLVardef@3c8452org.highwire.dtl.DTLVardef@11358f4org.highwire.dtl.DTLVardef@1352ae9org.highwire.dtl.DTLVardef@1943807_HPS_FORMAT_FIGEXP M_FIG C_FIG New & NoteworthyThis study introduces a frequency-domain analytical framework to quantify dynamic renal blood flow regulation after spinal cord injury (SCI). By resolving myogenic and sympathetic vasomotor activity across physiologically relevant frequency bands, we reveal that high-thoracic SCI causes a sustained, broadband loss of renal vasomotion and impaired autoregulatory responses to acute hypertension. In contrast, low-thoracic SCI preserves baseline spectral activity and permits recovery over time. This approach provides a mechanistic link between autonomic disruption and renal vascular dysfunction following SCI.