Premium
Rostral ventral lateral medulla (RVLM) mediates sympathetic vasomotor response to hypoglycemia
Author(s) -
Bardgett Megan Elyse,
Stocker Sean
Publication year - 2008
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.22.1_supplement.1169.2
Subject(s) - rostral ventrolateral medulla , vasomotor , medicine , endocrinology , hypoglycemia , insulin , saline , blood pressure , epinephrine , anesthesia , heart rate
Acute hypoglycemia or glucodeprivation increases vasomotor and non‐vasomotor sympathetic nerve activity (SNA). Neurons in RVLM are believed to mediate the increased non‐vasomotor SNA (increased epinephrine levels) seen following 2‐DG induced glucodeprivation but the neural pathway responsible for increases in vasomotor SNA has not been established. The primary goal of this study was to determine whether the increased renal SNA observed during insulin induced hypoglycemia is mediated by the RVLM. Hypoglycemia was achieved in anaesthetized male Sprague Dawley rats (300–450g) by a bolus injection of insulin (0.25U/kg) followed by insulin infusion (7.5 mU/kg/min) for 120 minutes. Insulin decreased blood glucose from 85±5 to 40±1 mg/dl (n=8). Renal SNA significantly increased in response to insulin but not saline infusion (140±10% vs 105±9% respectively) after 75 minutes, while blood pressure did not significantly change. Then inhibition of the RVLM with bilateral injection of the GABAA agonist muscimol (500pmol/100nl) produced a greater reduction in renal SNA of rats infused with insulin vs saline (−90±10% vs −62±7% p<0.05). Injection of saline into RVLM did not affect the increase in renal SNA (137±9% at 75 minutes to 153±15% at 90 minutes). These findings indicate that RVLM neurons play a role in the increased vasomotor SNA during hypoglycemia.