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High Sodium Diet – Role in Renal Sympathodepression
Author(s) -
Rodionova Kristina,
Ditting Tilmann,
Fahrmeier Franziska,
Ott Christian,
Schmieder Roland,
Schiffer Mario,
Amann Kerstin,
Veelken Roland Albert
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.02841
Subject(s) - saline , medicine , endocrinology , tonic (physiology) , capsaicin , chemistry , trpv1 , receptor , transient receptor potential channel
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. 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 were equipped with femoral catheters for blood pressure (BP) & heart rate (HR) assessment, drug application, a renal arterial catheter for intrarenal administration (IRA) of NaCl boil (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. In neurons from rats on high salt diet, but not on 0.9 % saline or tap water, the relation of tonic highly active neurons to less active neurons shifted towards less active units (62% tonic neurons in a control group vs. 40% on high salt diet and 63% on saline, significant, p<0.05, z‐test, mean +/−SEM). However, cultured renal neurons from rats on 0.9% saline or on high salt diet exhibited increased action potential production upon stimulation (Controls 13,3+/11,03 APs/600ms vs. saline 19,8+/−2,33 APs/600ms vs. high salt diet 22,2+/−4,54 APs/600ms, significant, <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 (10% NaCl, p<0.05) impaired in rats on 8% NaCl chow. (Suppressed RSNA unmasked in all groups by an i.v. NK1‐inhibitor). In rats on high salt diet 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. The sodium inducible long‐lasting sympatho‐depression via a neuro‐humoral tachykinin mediated afferent renal nerve pathway got eventually impaired.