PVN SK channel blockade alters sympathetic burst characteristics and transduction in Sprague-Dawley rats

The paraventricular nucleus (PVN) of the hypothalamus serves as an integrative control center for sympathetic nerve activity (SNA). Small conductance Ca 2+ -activated K + (SK) channels serve as negative feedback regulators of neuronal excitability, and we’ve previously reported that PVN SK channel dysfunction contributes to sympathoexcitation in hypertension. Notably, the PVN regulates not only SNA, but its spectral content as well, by producing frequency specific patterns that promote cardiovascular homeostasis. Bursts of SNA cause norepinephrine release which will augment mean arterial pressure (MAP) in subsequent cardiac cycles. Therefore, the aim of this study was to examine renal SNA (RSNA)-MAP transduction before and after blocking PVN SK channels with apamin. We hypothesize that blocking SK channels in the PVN will augment MAP, RSNA, and RSNA-MAP transduction. All experiments were performed in ventilated, anesthetized (urethane 800mg/kg & α-chloralose 80mg/kg) male Sprague-Dawley control rats. RSNA signals were rectified and integrated, and burst were detected using standardized criteria. Statistical analysis was performed with 2-way ANOVA and paired t-tests. Results are expressed as mean±SE. Differences were considered statistically significant at a critical value of p< 0.05. PVN microinjection of the SK channel blocker apamin (12.5pmol, 50µL) significantly (p< 0.05) increased RSNA (Δ140±46%) and MAP (Δ33.5±8.9 mmHg) compared to baseline. In contrast, PVN microinjection of apamin significantly reduced RSNA burst frequency (baseline 2.49±0.31 vs. max 1.56±0.28 Hz; p< 0.05) and RSNA burst incidence (baseline 40.76±3.697 vs. max 26.24±3.626 burst/100 heart beats; p< 0.05). RSNA bursts occurring during the maximum response to apamin elicited significantly (treatment p< 0.05) greater increases in MAP in the following 12 cardiac cycles compared to burst that occurred during baseline. In conclusion, blocking SK channels in the PVN augments RSNA through mechanisms that do not include elevations in burst quantity, but result in increased RSNA-MAP transduction. Funding: Michigan Technological University Health Research Institute and the National Institutes of Health (1R15HL177713-01A1) This abstract was presented at the American Physiology Summit 2026 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.