Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats
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Data
2013
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Resumo
Neurons of the rostral ventrolateral
medulla (RVLM) are critical for generating and regulating
sympathetic nerve activity (SNA). Systemic administration of ANG II
combined with a high-salt diet induces hypertension that is postulated to
involve elevated SNA. However, a functional role for RVLM vasomotor
neurons in ANG II-salt hypertension has not been established. Here we
tested the hypothesis that RVLM vasomotor neurons have exaggerated
resting discharge in rats with ANG II-salt hypertension. Rats in the
hypertensive (HT) group consumed a high-salt (2% NaCl) diet and
received an infusion of ANG II (150 ng·kg 1·min 1 sc) for 14 days. Rats
in the normotensive (NT) group consumed a normal salt (0.4% NaCl) diet
and were infused with normal saline. Telemetric recordings in conscious
rats revealed that mean arterial pressure (MAP) was significantly increased
in HT compared with NT rats (P 0.001). Under anesthesia
(urethane/chloralose), MAP remained elevated in HT compared with NT
rats (P 0.01). Extracellular single unit recordings in HT (n 28) and
NT (n 22) rats revealed that barosensitive RVLM neurons in both
groups (HT, 23 cells; NT, 34 cells) had similar cardiac rhythmicity and
resting discharge. However, a greater (P 0.01) increase of MAP was
needed to silence discharge of neurons in HT (17 cells, 44 5 mmHg)
than in NT (28 cells, 29 3 mmHg) rats. Maximum firing rates during
arterial baroreceptor unloading were similar across groups. We conclude
that heightened resting discharge of sympathoexcitatory RVLM neurons
is not required for maintenance of neurogenic ANG II-salt hypertension.
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Palavras-chave
Angiotensin II, Sympathetic nerve activity, High-salt diet, Single unit recording, Hypertension, Rostral ventrolateral medulla vasomotor neurons
Citação
PEDRINO, Gustavo R. et al. Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats. American Journal of Physiology. Heart and Circulatory Physiology, Rockville, v. 305, n. 12, p. H1781-H1789, 2013.