Glutamate receptor activation in the rostral ventrolateral medulla (RVLM) mediates the sympathetic response to increased cerebrospinal fluid (CSF) sodium concentration
Beschreibung:
<jats:p>Compelling evidence indicates increased CSF sodium concentration elevates sympathetic nerve activity (SNA) and arterial blood pressure (ABP) in salt‐sensitive hypertension. RVLM neurons project to the spinal cord and regulate SNA and ABP under a number of physiological challenges and pathophysiological states. Therefore, we hypothesized that RVLM neurons mediate the sympathoexcitatory response to increased CSF sodium. Inactin‐anesthetized, male Sprague‐Dawley rats (n=5/group) were infused with 1M NaCl (5 μL/10 min) or artificial CSF in the lateral ventricle and then received an RVLM injection (60 nL) of CSF or the ionotropic glutamate receptor antagonist kynurenic acid (KYN, 25 mM). Infusion of 1M NaCl significantly increased lumbar SNA (112±1%, P<0.05) and ABP (Δ: 9±1 mmHg, P<0.05). RVLM injection of KYN significantly attenuated (P<0.05) the increase in lumbar SNA (101±3%) and mean ABP (Δ: 1±2 mmHg). In addition, in vivo single‐unit recordings demonstrate that infusion of 1M NaCl increased discharge in 60% (3/5) of spinally‐projecting, barosensitive RVLM neurons (2.1±0.4 to 5.8±0.2 Hz, P<0.05). These findings suggest increased CSF sodium activates RVLM neurons to elevate SNA and ABP.</jats:p>