Sympathetic Transduction in Sprague-Dawley Rats: A Methodological Tool for Translational Studies

Introduction: Cardiovascular disease (CVD) is the leading cause of death in the United States. CVD is associated with elevations in sympathetic nerve activity (SNA), which impact the vasculature both acutely and chronically. In human studies, the ability of SNA to vasoconstrict has been examined by a signal averaging methodology assessing beat-to-beat changes in blood pressure (BP) following spontaneous bursts of SNA (i.e. sympathetic transduction to BP). Whether sympathetic transduction to BP analysis can be applied in rodent models is unknown, particularly given higher heart rates and SNA burst frequencies than humans. PURPOSE: The purpose of this study was to investigate rodent sympathetic transduction to BP using analyses which we have previously implemented in human nerve transduction research. Hypothesis: We hypothesized that sympathetic transduction would influence the vasculature in a more rapid timeframe in rodents compared to humans and that burst amplitude and burst clustering would alter the magnitude of BP responses. Methods: In recordings from Inactin-anesthetized rats (n=9, age 4-16 weeks, 6 female), we analyzed baseline, beat-to-beat mean arterial pressure (MAP) from an indwelling catheter and splanchnic SNA using silver, bipolar electrodes implanted with polyvinyl siloxane gel. SNA was rectified and integrated in LabChart software, and sympathetic transduction to BP was calculated using a customized Excel spreadsheet, modified from studies performed in humans. Briefly, SNA recordings were analyzed on a cardiac cycle basis, and each event was tracked for 30 cardiac cycles. Bursts were categorized based on occurrence pattern (i.e., in isolation versus in sequences of 2 or more consecutive bursts). Burst heights were normalized to the average of the three highest amplitudes, and bursts were sorted into quartiles (e.g., Q1 = smallest 25% of bursts, Q4 = largest 25% of bursts). Results: On average, SNA bursts which occurred in clusters of 2 or more consecutive bursts resulted in a peak increase in MAP of 1.1±0.6 mmHg (range: 0.06 to 5.2 mmHg). Conversely, cardiac cycles not associated with SNA bursts were followed by a nadir decrease in MAP of -1.2±0.4 mmHg (range: -0.05 to -2.8 mmHg). When bursts were placed into height quartiles, those with the lowest amplitude (Q1) resulted in minimal changes in MAP (peak: 0.5±0.2 mmHg; range: 0.05 to 1.8 mmHg), whereas those with the highest amplitude (Q4) produced a more robust increase in MAP (peak: 2.1±0.9 mmHg; range: 0.1 to 7.5 mmHg). Conclusion: Ourpreliminary results suggest sympathetic transduction to BP analysis may be used as a translational tool in rodents. However, these initial findings also highlight the variability of BP responses following SNA bursts and indicate a need for further exploration and standardization. Supported by HL161233 (PJM). This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.