Abstract: TH-PO0281
Sympathoinhibitory Afferent Nerve Pathways from the Kidneys in Rats: Physiological and Pathophysiological Effects of Sodium
Session Information
- Hypertension and CVD: Mechanisms
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1601 Hypertension and CVD: Basic
Authors
- Rodionova, Kristina, Friedrich-Alexander-Universitat Erlangen-Nurnberg Medizinische Fakultat, Erlangen, BY, Germany
- Ditting, Tilmann, Friedrich-Alexander-Universitat Erlangen-Nurnberg Medizinische Fakultat, Erlangen, BY, Germany
- Hilgers, Karl F., Friedrich-Alexander-Universitat Erlangen-Nurnberg Medizinische Fakultat, Erlangen, BY, Germany
- Schmieder, Roland E., Friedrich-Alexander-Universitat Erlangen-Nurnberg Medizinische Fakultat, Erlangen, BY, Germany
- Schiffer, Mario, Friedrich-Alexander-Universitat Erlangen-Nurnberg Medizinische Fakultat, Erlangen, BY, Germany
- Amann, Kerstin U., Friedrich-Alexander-Universitat Erlangen-Nurnberg Medizinische Fakultat, Erlangen, BY, Germany
- Veelken, Roland, Friedrich-Alexander-Universitat Erlangen-Nurnberg Medizinische Fakultat, Erlangen, BY, Germany
Background
High salt diets might impair afferent renal nerve pathways increasing renal sympathetic nerve activity (RSNA) in hypertension. We reported previously on a specific long lasting sympatho-inhibitiory reflex depending on TRPV1 receptors elicited by intrarenal afferent nerve stimulation. We wanted to test the hypothesis that sodium influences this renal afferent sympatho-depressory mechanism impaired during high salt diet.
Methods
Rats were put on a normal diet or a high rat chow containing 8% NaCl, later equipped with femoral catheters (blood pressure (BP) & heart rate (HR)), a renal arterial catheter for intrarenal administration (IRA) of high salt boli (10 % NaCl, 10 µl) or the TRPV 1 receptor agonist capsaicin (CAP 3.3, 6.6, 10, 33*10-7 M, 10 µl) and bipolar electrode for RSNA recordings. Cultured dorsal root ganglion neurons (Th11-L2) of rats with renal afferents were investigated in current clamp mode to assess action potential generation or in voltage clamp mode to investigate inward currents during 10 sec exposure to 4.5 % NaCl. Results are given in mean±SEM.
Results
IRA with high salt or IRA CAP boli decreased RSNA from baseline 4.1±0.6 µV*sec to 2.2±0.8 µV*sec (10% NaCl, p<0.05) and 3.9±0.5 µV*sec to 0.9±0.2 µV*sec (CAP, p<0.01).
Interestingly, suppressed RSNA in groups renally injected with high salt boli or CAP could be unmasked by the systemic administration of the tachykinin NK1-blocker RP67580 (10*10-3M, 15 μl).
Decreases of RSNA due 10% NaCl boli were impaired after high salt chow.
Renal neurons produced action potentials (3.5±0.8, *p<0.05) during exposure to NaCl 4.5 %. In neurons from rats on a high salt diet, the relation of tonic highly active neurons to less active neurons shifted towards the latter. (tap water -tonic/phasic: 22/15; saline - tonic/phasic: 28/18; 8% high salt - tonic/phasic: 14/21* P<0.05).
Conclusion
Increased intrarenal sodium concentrations likely induce long-lasting sympatho-depression via a neuro-humoral TRPV1 dependent, and tachykinin mediated afferent renal nerve pathways. However, this mechanism is impaired during increased ingestion of sodium chloride: the control of RSNA is weakened while the afferent pathways exhibit a reduced number of highly active neurons.
Funding
- Other NIH Support