Abstract: TH-PO0057
Loss of Renal Interoceptive Input Reduces Salt Appetite in Response to Acute Fluid and Sodium Loss
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Basic Research
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1101 Fluid, Electrolyte, and Acid-Base Disorders: Basic
Authors
- Anidu, Babatunde Shuaib, University of Minnesota Twin Cities, Minneapolis, Minnesota, United States
- Almutlaq, Rawan N., University of Minnesota Twin Cities, Minneapolis, Minnesota, United States
- Ruiz Lauar, Mariana, University of Minnesota Twin Cities, Minneapolis, Minnesota, United States
- Dayton, Alexander R., University of Minnesota Twin Cities, Minneapolis, Minnesota, United States
- Evans, Louise Christine, University of Minnesota Twin Cities, Minneapolis, Minnesota, United States
Background
Sodium depletion stimulates salt appetite, in part through rising levels of angiotensin II and aldosterone, but the peripheral signals driving this response remain unclear. We previously showed that disrupting afferent renal nerves reduces salt appetite in DOCA-salt rats. Here, we tested whether afferent renal nerves are required for sodium appetite following acute sodium and volume depletion. We hypothesized that selective ablation of afferent renal nerves would reduce sodium intake under these conditions.
Methods
Female Sprague-Dawley rats (Sham n = 5; afferent renal denervation (ARDN) n = 6; total renal denervation (TRDN) n = 4) were implanted with radiotelemetry transmitters and housed individually with ad libitum access to water and chow. Acute sodium and fluid depletion was induced with furosemide (10 mg/kg, s.c.) followed 10 minutes later by captopril (5 mg/kg, s.c.). During the 60-minute depletion period, rats did not have access to food or water. After 60 minutes, rats received a two-bottle choice of dH2O and 1.8% NaCl, and intake was measured at 30, 60, 90, and 120 minutes. Data were analyzed using a linear mixed model and one-way ANOVA with Tukey’s post hoc test.
Results
Following sodium depletion, sham rats consumed markedly more saline than both ARDN and TRDN rats during the 2-hour test (18.7 vs. 3.6 vs. 2.9 mL/100 g BW; P < 0.05), with no difference between denervation groups. Water intake was comparable across all groups. In a separate depletion challenge during which rats were housed in metabolic cages, ARDN and TRDN rats lost more body weight and produced more urine than sham rats (both P < 0.05), with no difference between ARDN and TRDN. Plasma sodium and potassium concentrations were similar across sham, ARDN, and TRDN groups (Na+: 140.35, 138.10, 137.58 mmol/L; K+: 4.31, 4.39, 4.62 mmol/L, P > 0.05 respectively).
Conclusion
These findings indicate that interoceptive input from the kidney to the brain contributes to sodium appetite in response to acute sodium depletion, as selective ARDN reduced saline intake without altering water intake or electrolyte balance. Future studies will use fiber photometry to identify brain regions activated during sodium depletion and determine how renal afferent signaling shapes the neural circuits that drive salt appetite.
Acknowledgment
LE is funded by R01HL152166.
Funding
- Other NIH Support