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Lumbar denervation attenuates the sympathetic‐cardiovascular response to acute increases in cerebrospinal fluid sodium concentration
Author(s) -
Simmonds Sarah Shayne,
Stocker Sean D.
Publication year - 2013
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.27.1_supplement.lb731
Subject(s) - medicine , heart rate , lumbar , mean arterial pressure , denervation , anesthesia , blood pressure , splanchnic , cerebrospinal fluid , sympathetic nervous system , endocrinology , hemodynamics , anatomy
Increased concentration of sodium in cerebral spinal fluid elevates sympathetic nerve activity (SNA), heart rate (BPM), and mean arterial pressure (MAP). The present study aims to identify the contribution of the sympathetic nervous system to this response. In anaesthetized male Sprague Dawley rats, infusion of 1M NaCl (5μL/10min) into the lateral ventricle increased MAP (Δ 7±1 mmHg), heart rate (Δ 14±4 BPM), lumbar SNA (Δ 115±3%), splanchnic SNA (Δ117±4%) and adrenal SNA(Δ111±3%) but decreased renal SNA (Δ 89±3%). Pretreatment with the ganglionic blocker chlorisondamine (5mg/kg, IV) prevented the rise in MAP(Δ1±1mmHg) and heart rate (Δ4±3BPM). In a final set of experiments, the increase in MAP was significantly attenuated by lumbar denervation (area under the curve: control 5.3±0.8; lumbar 3.1±1.0) but unaffected by renal denervation (area under the curve: 5.6±1.5) or celiac ganglionectomy (area under the curve: 7.1±2.0). These findings indicate that an increase in sodium concentration in cerebral spinal fluid activates the lumbar nerve, at least partly, to increase MAP and heart rate.