Abstract: SA-PO317
High Sodium Intake Impairs Afferent Renal Sympatho-Depressory Pathways in Rats
Session Information
- Hypertension and CVD: Mechanisms
November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Hypertension and CVD
- 1403 Hypertension and CVD: Mechanisms
Authors
- Rodionova, Kristina, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Fahrmeier, Franziska, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Ott, Christian, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Schmieder, Roland E., Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Schiffer, Mario, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Amann, Kerstin U., Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Veelken, Roland, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
- Ditting, Tilmann, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany
Background
Afferent renal nerve pathways are likely involved in the development of salt sensitive hypertension. We recently reported that intrarenal NaCl elicited a long-lasting sympatho-depression via a neuro-humoral TRPV1 dependent and tachykinin mediated renal afferent nerve pathway. We now wanted to test the hypothesis that high sodium intake impairs this afferent sympatho-depressory mechanism.
Methods
Respective groups were put on tap water, 0.9 % saline for drinking or chow containing 8% NaCl. Cultured dorsal root ganglion neurons (DRG Th11-L2) of rats with renal afferents were investigated in current clamp mode to assess action potential generation during current injection. Rats with femoral catheters for blood pressure (BP) & heart rate (HR) assessment, drug application, a renal arterial catheter for intrarenal administration (IRA) of NaCl boli (10 % NaCl, 10 μl) or Capsaicin (CAP 3.3, 6.6, 10, 33*10-7 M, 10 μl) and a bipolar electrode for renal sympathetic nerve activity (RSNA) recordings; eventually an intravenous (iv) bolus of the NK1-receptor blocker RP67580 (10*10-3M, 15 μl) was administered. Results are mean±SEM.
Results
In neurons from rats on 8% NaCl, but not on 0.9 % saline or controls the relation of tonic highly active neurons to less active neurons shifted towards less active units. (62% tonic neurons in the control group and 63% tonic neurons in the saline group vs. 40%* tonic neurons in the high salt group, * p<0.05, z-test, mean +/-SEM). However, cultured renal neurons from rats on 0,9% saline or on 8% NaCl exhibited increased action potential production upon stimulation (controls 13,3+/11,03 APs/600ms vs. 0.9% saline 19,8+/-2,33* APs/600ms vs. high salt diet 22,2+/-4,54 APs/600ms, * p<0.05, t-test, mean+/-SEM). 10% NaCl boli IRA induced decreases of RSNA from baseline 4.1±0.6 μV*sec to 2.2±0.8 μV*sec impaired in rats on 8% NaCl. (Suppressed RSNA by an i.v. NK1-inhibitor).
Conclusion
In rats on a high salt diet the number of highly active tonic neurons with renal afferents in vitro decreased at the expense of less active phasic neurons in spite of tonic neurons producing more action potentials upon stimulation in the group on 8% NaCl. The sodium inducible long-lasting sympatho-depression via a neuro-humoral tachykinin mediated afferent renal nerve pathway was eventually impaired.