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MODULATION OF RVLM VASOMOTOR NEURON DISCHARGE IN ANGIOTENSIN II ‐ SALT HYPERTENSIVE RATS
Author(s) -
Toney Glenn M,
Alvarado Steven R,
Calderon Alfred S
Publication year - 2007
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.21.6.a891-b
Subject(s) - rostral ventrolateral medulla , medicine , vasomotor , endocrinology , angiotensin ii , antidromic , neuron , chemistry , blood pressure , heart rate , cardiology , electrophysiology , psychiatry
Elevated angiotensin II (ANG II) and dietary salt (NaCl) increase sympathetic outflow and arterial pressure. In rats consuming a 2% NaCl diet and treated with ANG II (150 ng/kg/min, s.c.) for 2 wks (n=21), MAP increased from 104 ± 2.3 mmHg to a plateau of 135 ± 4.9 mmHg from days 6–14. Extracellular recording and spinal (T2–3) antidromic activation were used to identify RVLM vasomotor neurons in anesthetized rats and to assess effects of ANG II + salt on their discharge. Among cells with relatively fast (>2.5 m/s) axonal conduction velocity (CV), firing rate in hypertensive rats averaged 5.6 ± 2.4 Hz (n=14) compared to 1.8 ± 0.9 Hz in untreated controls (n=7). Cells discharging with a cardiac rhythm at resting MAP had basal firing rates that did not differ across groups. Nevertheless, R‐wave triggered phase analysis revealed that peak discharge during the cardiac cycle was delayed in cells from hypertensive rats (59 ± 6 %, n=6) compared to controls (40 ± 13%, n=6). Moreover, raising MAP silenced cells from hypertensive rats at higher MAP (186 ± 13 mmHg, n=5) than controls (150 ± 7 mmHg, n=5) (p<0.05). We conclude that ANG II + salt treatment increases the discharge of RVLM neurons with myelinated spinal axons, delays temporal coupling of baro‐entrainment and blunts responses to increased MAP. These effects could reflect modulation of RVLM neurons, plasticity at antecedent synapses or both. Identification of underlying mechanisms could lend insight into the development of novel antihypertensive treatments. Support: HL076312 (NCDC)